@article{simoes_lavoy_dean_2019, title={Effects of Regulatory T Cell Depletion on NK Cell Responses against Listeria monocytogenes in Feline Immunodeficiency Virus Infected Cats}, volume={11}, ISSN={["1999-4915"]}, DOI={10.3390/v11110984}, abstractNote={Regulatory T cells (Treg) are key players in the maintenance of peripheral tolerance, preventing autoimmune diseases and restraining chronic inflammatory diseases. Evidence suggests Treg cells and NK cells have important roles in feline immunodeficiency virus (FIV) pathogenesis; however, in vivo studies investigating the interplay between these two cell populations are lacking. We previously described innate immune defects in FIV-infected cats characterized by cytokine deficits and impaired natural killer cell (NK) and NK T cell (NKT) functions. In this study, we investigated whether in vivo Treg depletion by treatment with an anti-feline CD25 monoclonal antibody would improve the innate immune response against subcutaneous challenge with Listeria monocytogenes (Lm). Treg depletion resulted in an increased overall number of cells in Lm-draining lymph nodes and increased proliferation of NK and NKT cells in FIV-infected cats. Treg depletion did not normalize expression of perforin or granzyme A by NK and NKT cells, nor did Treg depletion result in improved clearance of Lm. Thus, despite the quantitative improvements in the NK and NKT cell responses to Lm, there was no functional improvement in the early control of Lm. CD1a+ dendritic cell percentages in the lymph nodes of FIV-infected cats were lower than in specific-pathogen-free control cats and failed to upregulate CD80 even when Treg were depleted. Taken together, Treg depletion failed to improve the innate immune response of FIV-infected cats against Lm and this may be due to dendritic cell dysfunction.}, number={11}, journal={VIRUSES-BASEL}, author={Simoes, Rita D. and LaVoy, Alora and Dean, Gregg A.}, year={2019}, month={Nov} }
 @article{kajikawa_zhang_long_nordone_stoeker_lavoy_bumgardner_klaenhammer_dean_2012, title={Construction and Immunological Evaluation of Dual Cell Surface Display of HIV-1 Gag and Salmonella enterica Serovar Typhimurium FliC in Lactobacillus acidophilus for Vaccine Delivery}, volume={19}, ISSN={["1556-6811"]}, DOI={10.1128/cvi.00049-12}, abstractNote={ABSTRACT}, number={9}, journal={CLINICAL AND VACCINE IMMUNOLOGY}, author={Kajikawa, Akinobu and Zhang, Lin and Long, Julie and Nordone, Shila and Stoeker, Laura and LaVoy, Alora and Bumgardner, Sara and Klaenhammer, Todd and Dean, Gregg}, year={2012}, month={Sep}, pages={1374–1381} }
 @article{simoes_howard_dean_2012, title={In Vivo Assessment of Natural Killer Cell Responses during Chronic Feline Immunodeficiency Virus Infection}, volume={7}, ISSN={["1932-6203"]}, DOI={10.1371/journal.pone.0037606}, abstractNote={Accumulating evidence suggests that natural killer (NK) cells may have an important role in HIV-1 disease pathogenesis; however, in vivo studies are lacking. Feline immunodeficiency virus (FIV) infection of cats provides a valuable model to study NK cell function in vivo. The immune response against Listeria monocytogenes (Lm) is well characterized, allowing its use as an innate immune probe. We have previously shown that locally delivered IL-15 can improve Lm clearance in FIV-infected animals, and this correlated with an increase in NK cell number. In the present study, chronically FIV-infected and SPF-control cats were challenged with Lm by unilateral subcutaneous injection next to the footpad and then treated with 5-bromo-2′-deoxyuridine (BrdU). The Lm draining and contralateral control lymph nodes were evaluated for NK, NKT, CD4+ and CD8+ T cell number, proliferation, apoptosis, and NK cell function. Listeria monocytogenes burden was also assessed in both control and Lm draining lymph nodes. NK, NKT, CD4+ T and CD8+ T cells in the Lm-challenged lymph node of FIV-infected cats did not increase in number. In addition, after Lm challenge, NK cells from FIV-infected cats did not increase their proliferation rate, apoptosis was elevated, and perforin expression was not upregulated when compared to SPF-control cats. The failure of the NK cell response against Lm challenge in the draining lymph node of FIV-infected cats correlates with the delayed control and clearance of this opportunistic bacterial pathogen.}, number={5}, journal={PLOS ONE}, author={Simoes, Rita D. and Howard, Kristina E. and Dean, Gregg A.}, year={2012}, month={May} }
 @article{stoeker_nordone_gunderson_zhang_kajikawa_lavoy_miller_klaenhammer_dean_2011, title={Assessment of Lactobacillus gasseri as a Candidate Oral Vaccine Vector}, volume={18}, ISSN={["1556-6811"]}, DOI={10.1128/cvi.05277-11}, abstractNote={ABSTRACT}, number={11}, journal={CLINICAL AND VACCINE IMMUNOLOGY}, author={Stoeker, Laura and Nordone, Shila and Gunderson, Sara and Zhang, Lin and Kajikawa, Akinobu and LaVoy, Alora and Miller, Michael and Klaenhammer, Todd R. and Dean, Gregg A.}, year={2011}, month={Nov}, pages={1834–1844} }
 @article{kajikawa_nordone_zhang_stoeker_lavoy_klaenhammer_dean_2011, title={Dissimilar Properties of Two Recombinant Lactobacillus acidophilus Strains Displaying Salmonella FliC with Different Anchoring Motifs}, volume={77}, ISSN={["0099-2240"]}, DOI={10.1128/aem.05153-11}, abstractNote={ABSTRACT}, number={18}, journal={APPLIED AND ENVIRONMENTAL MICROBIOLOGY}, author={Kajikawa, Akinobu and Nordone, Shila K. and Zhang, Lin and Stoeker, Laura L. and LaVoy, Alora S. and Klaenhammer, Todd R. and Dean, Gregg A.}, year={2011}, month={Sep}, pages={6587–6596} }
 @article{wendelsdorf_dean_hu_nordone_banks_2011, title={Host immune responses that promote initial HIV spread}, volume={289}, ISSN={["1095-8541"]}, DOI={10.1016/j.jtbi.2011.08.012}, abstractNote={The host inflammatory response to HIV invasion is a necessary component of the innate antiviral activity that vaccines and early interventions seek to exploit/enhance. However, the response is dependent on CD4+ T-helper cell 1 (Th1) recruitment and activation. It is this very recruitment of HIV-susceptible target cells that is associated with the initial viral proliferation. Hence, global enhancement of the inflammatory response by T-cells and dendritic cells will likely feed viral propagation. Mucosal entry sites contain inherent pathways, in the form of natural regulatory T-cells (nTreg), that globally dampen the inflammatory response. We created a model of this inflammatory response to virus as well as inherent nTreg-mediated regulation of Th1 recruitment and activation. With simulations using this model we sought to address the net effect of nTreg activation and its specific functions as well as identify mechanisms of the natural inflammatory response that are best targeted to inhibit viral spread without compromising initial antiviral activity. Simulation results provide multiple insights that are relevant to developing intervention strategies that seek to exploit natural immune processes: (i) induction of the regulatory response through nTreg activation expedites viral proliferation due to viral production by nTreg itself and not to reduced Natural Killer (NK) cell activity; (ii) at the same time, induction of the inflammation response through either DC activation or Th1 activation expedites viral proliferation; (iii) within the inflammatory pathway, the NK response is an effective controller of viral proliferation while DC-mediated stimulation of T-cells is a significant driver of viral proliferation; and (iv) nTreg-mediated DC deactivation plays a significant role in slowing viral proliferation by inhibiting T-cell stimulation, making this function an aide to the antiviral immune response.}, journal={JOURNAL OF THEORETICAL BIOLOGY}, author={Wendelsdorf, K. and Dean, G. and Hu, Shuhua and Nordone, S. and Banks, H. T.}, year={2011}, month={Nov}, pages={17–35} }
 @article{mikkelsen_long_zhang_galemore_vandewoude_dean_2011, title={Partial Regulatory T Cell Depletion Prior to Acute Feline Immunodeficiency Virus Infection Does Not Alter Disease Pathogenesis}, volume={6}, ISSN={["1932-6203"]}, DOI={10.1371/journal.pone.0017183}, abstractNote={Feline immunodeficiency virus (FIV) infection in cats follows a disease course similar to HIV-1, including a short acute phase characterized by high viremia, and a prolonged asymptomatic phase characterized by low viremia and generalized immune dysfunction. CD4+CD25hiFoxP3+ immunosuppressive regulatory T (Treg) cells have been implicated as a possible cause of immune dysfunction during FIV and HIV-1 infection, as they are capable of modulating virus-specific and inflammatory immune responses. Additionally, the immunosuppressive capacity of feline Treg cells has been shown to be increased during FIV infection. We have previously shown that transient in vivo Treg cell depletion during asymptomatic FIV infection reveals FIV-specific immune responses suppressed by Treg cells. In this study, we sought to determine the immunological influence of Treg cells during acute FIV infection. We asked whether Treg cell depletion prior to infection with the highly pathogenic molecular clone FIV-C36 in cats could alter FIV pathogenesis. We report here that partial Treg cell depletion prior to FIV infection does not significantly change provirus, viremia, or CD4+ T cell levels in blood and lymphoid tissues during the acute phase of disease. The effects of anti-CD25 mAb treatment are truncated in cats acutely infected with FIV-C36 as compared to chronically infected cats or FIV-naïve cats, as Treg cell levels were heightened in all treatment groups included in the study within two weeks post-FIV infection. Our findings suggest that the influence of Treg cell suppression during FIV pathogenesis is most prominent after Treg cells are activated in the environment of established FIV infection.}, number={2}, journal={PLOS ONE}, author={Mikkelsen, S. Rochelle and Long, Julie M. and Zhang, Lin and Galemore, Erin R. and VandeWoude, Sue and Dean, Gregg A.}, year={2011}, month={Feb} }
 @article{howard_reckling_egan_dean_2010, title={Acute mucosal pathogenesis of feline immunodeficiency virus is independent of viral dose in vaginally infected cats}, volume={7}, ISSN={["1742-4690"]}, DOI={10.1186/1742-4690-7-2}, abstractNote={The mucosal pathogenesis of HIV has been shown to be an important feature of infection and disease progression. HIV-1 infection causes depletion of intestinal lamina propria CD4+ T cells (LPL), therefore, intestinal CD4+ T cell preservation may be a useful correlate of protection in evaluating vaccine candidates. Vaccine studies employing the cat/FIV and macaque/SIV models frequently use high doses of parenterally administered challenge virus to ensure high plasma viremia in control animals. However, it is unclear if loss of mucosal T cells would occur regardless of initial viral inoculum dose. The objective of this study was to determine the acute effect of viral dose on mucosal leukocytes and associated innate and adaptive immune responses. Cats were vaginally inoculated with a high, middle or low dose of cell-associated and cell-free FIV. PBMC, serum and plasma were assessed every two weeks with tissues assessed eight weeks following infection. We found that irrespective of mucosally administered viral dose, FIV infection was induced in all cats. However, viremia was present in only half of the cats, and viral dose was unrelated to the development of viremia. Importantly, regardless of viral dose, all cats experienced significant losses of intestinal CD4+ LPL and CD8+ intraepithelial lymphocytes (IEL). Innate immune responses by CD56+CD3- NK cells correlated with aviremia and apparent occult infection but did not protect mucosal T cells. CD4+ and CD8+ T cells in viremic cats were more likely to produce cytokines in response to Gag stimulation, whereas aviremic cats T cells tended to produce cytokines in response to Env stimulation. However, while cell-mediated immune responses in aviremic cats may have helped reduce viral replication, they could not be correlated to the levels of viremia. Robust production of anti-FIV antibodies was positively correlated with the magnitude of viremia. Our results indicate that mucosal immune pathogenesis could be used as a rapid indicator of vaccine success or failure when combined with a physiologically relevant low dose mucosal challenge. We also show that innate immune responses may play an important role in controlling viral replication following acute mucosal infection, which has not been previously identified.}, journal={RETROVIROLOGY}, author={Howard, Kristina E. and Reckling, Stacie K. and Egan, Erin A. and Dean, Gregg A.}, year={2010}, month={Jan} }
 @article{mikkelsen_reckling_egan_dean_2010, title={In vivo depletion of CD4(+)CD25(hi) regulatory T cells is associated with improved antiviral responses in cats chronically infected with feline immunodeficiency virus}, volume={403}, ISSN={["0042-6822"]}, DOI={10.1016/j.virol.2010.04.016}, abstractNote={Regulatory T (Treg) cells are activated and suppress immune responses during infection, and are characterized as CD4+CD25hiFOXP3+. Ex vivo studies demonstrate that Treg cells potentially suppress anti-HIV-1 T cell responses. Lentivirus-induced CD4+CD25hi Treg cells were first described in feline immunodeficiency virus (FIV)-infected cats. In the present study we demonstrate that anti-feline CD25 monoclonal antibody (mAb) therapy depletes Treg cells in FIV-infected cats for 4 weeks and does not exacerbate viral replication or proinflammatory cytokine production. Significant FIV-specific immune responses are revealed in Treg cell-depleted cats. These anti-FIV effector cells exist prior to Treg cell depletion and are not expanded while Treg cells are depleted. Importantly, cats receiving the Treg cell-depleting mAb are able to produce a robust humoral response to new antigen. We propose that short-term in vivo Treg cell depletion during chronic HIV-1 infection could provide a window of opportunity for therapeutic vaccination in individuals with controlled viral replication.}, number={2}, journal={VIROLOGY}, author={Mikkelsen, S. Rochelle and Reckling, Stacie K. and Egan, Erin A. and Dean, Gregg A.}, year={2010}, month={Aug}, pages={163–172} }
 @article{lehman_kevin p. o'halloran_fallon_habermann_campbell_nordone_dean_hoover_avery_2009, title={Altered bone marrow dendritic cell cytokine production to toll-like receptor and CD40 ligation during chronic feline immunodeficiency virus infection}, volume={126}, ISSN={["1365-2567"]}, DOI={10.1111/j.1365-2567.2008.02907.x}, abstractNote={Summary}, number={3}, journal={IMMUNOLOGY}, author={Lehman, Tracy L. and Kevin P. O'Halloran and Fallon, Samantha A. and Habermann, Lindsey M. and Campbell, Jennifer A. and Nordone, Shila and Dean, Gregg A. and Hoover, Edward A. and Avery, Paul R.}, year={2009}, month={Mar}, pages={405–412} }
 @article{gunderson_nordone_lavoy_zhang_klaenhammer_dean_2009, title={Immunogenicity of Lactobacillus gasseri-FliC as an oral mucosal vaccine adjuvant for HIV}, volume={6}, ISSN={["1742-4690"]}, DOI={10.1186/1742-4690-6-s3-p163}, abstractNote={Background Transmission of HIV-1 across mucosal surfaces is the most prevalent mode of viral infection. Therefore, a successful vaccine must induce broad anti-viral immunity at the mucosal surface. In the present study, we investigated the immunogenicity of a novel Lactobacillus gasseri mucosal vaccine vector for use in oral delivery of HIV antigens. L. gasseri was genetically engineered to express Salmonella spp. flagellin (L. gasseri-FliC) – the agonist for Toll-like receptor 5 (TLR5) and a potent activator of innate immune cells.}, journal={RETROVIROLOGY}, author={Gunderson, S. and Nordone, S. and LaVoy, A. and Zhang, L. and Klaenhammer, T. and Dean, G.}, year={2009} }
 @article{zimmerman_waters_lyashchenko_nonnecke_armstrong_jacobs_larsen_egan_dean_2009, title={Safety and Immunogenicity of the Mycobacterium tuberculosis Delta lysA Delta panCD Vaccine in Domestic Cats Infected with Feline Immunodeficiency Virus}, volume={16}, ISSN={["1556-6811"]}, DOI={10.1128/CVI.00396-08}, abstractNote={ABSTRACT}, number={3}, journal={CLINICAL AND VACCINE IMMUNOLOGY}, author={Zimmerman, Dawn M. and Waters, W. Ray and Lyashchenko, Konstantin P. and Nonnecke, Brian J. and Armstrong, Douglas L. and Jacobs, William R., Jr. and Larsen, Michelle H. and Egan, Erin and Dean, Gregg A.}, year={2009}, month={Mar}, pages={427–429} }
 @article{stoeker_nordone_lavoy_tallon_klaenhammer_dean_2009, title={Toll-like receptor activation profiles of wild-type, recombinant, and mutant Lactobacillus: implications for vaccine design}, volume={6}, ISSN={["1742-4690"]}, DOI={10.1186/1742-4690-6-s3-p133}, journal={RETROVIROLOGY}, author={Stoeker, L. and Nordone, S. and LaVoy, A. and Tallon, R. and Klaenhammer, T. and Dean, G.}, year={2009} }
 @article{maksaereekul_dubie_shen_kieu_dean_sparger_2009, title={Vaccination with vif-deleted feline immunodeficiency virus provirus, GM-CSF, and TNF-alpha plasmids preserves global CD4 T lymphocyte function after challenge with FIV}, volume={27}, ISSN={["1873-2518"]}, DOI={10.1016/j.vaccine.2009.03.081}, abstractNote={Feline immunodeficiency virus (FIV) DNA vaccine approaches that included a vif-deleted FIV provirus (FIV-pPPRΔvif) and feline cytokine expression plasmids were tested for immunogenicity and efficacy by immunization of specific pathogen free cats. Vaccine protocols included FIV-pPPRΔvif plasmid alone; a combination of FIV-pPPRΔvif DNA and feline granulocyte macrophage-colony stimulating factor (GM-CSF) and tumor necrosis factor (TNF)-α expression plasmids; or a combination of FIV-pPPRΔvif and feline interleukin (IL)-15 plasmids. Cats immunized with FIV-pPPRΔvif, GM-CSF and TNF-α plasmids demonstrated an increased frequency of FIV-specific T cell proliferation responses compared to other vaccine groups. Immunization with FIV-pPPRΔvif and IL-15 plasmids was distinguished from other vaccine protocols by the induction of antiviral antibodies. Suppression of virus loads was not observed for any of the FIV-pPPRΔvif DNA vaccine protocols after challenge with the FIV-PPR isolate. However, prior immunization with FIV-pPPRΔvif, GM-CSF, and TNF-α plasmids resulted in preservation of CD4 T cell functions, including mitogen-induced cytokine expression and antigen-specific proliferation upon infection with FIV. These findings justify further examination of cytokine combinations as adjuvants for lentiviral DNA vaccines.}, number={28}, journal={VACCINE}, author={Maksaereekul, Saipiroon and Dubie, Robert A. and Shen, Xiaoying and Kieu, Hung and Dean, Gregg A. and Sparger, Ellen E.}, year={2009}, month={Jun}, pages={3754–3765} }
 @article{renschler_dean_2009, title={What is your diagnosis? Abdominal mass aspirate in a cat with an increased Na:K ratio}, volume={38}, ISSN={["1939-165X"]}, DOI={10.1111/j.1939-165X.2008.00090.x}, abstractNote={Abstract:  A 13‐year‐old domestic shorthair cat was presented for evaluation of pollakiuria. Laboratory abnormalities included mild hypercholesterolemia, moderate hypertriglyceridemia, and a mild increase in the Na:K ratio (43, reference interval 32–41). Abdominal ultrasonography revealed urinary calculi and a soft tissue mass between the right caudate liver lobe and the right kidney. Surgery was done to remove the cystic calculi, and aspirates of the mass were obtained. Cytologic specimens contained a population of large, round to angular cells with round nuclei, coarse irregularly stippled chromatin, 1–2 prominent round to angular nucleoli, and abundant pale basophilic cytoplasm distended by numerous well‐delineated vacuoles. Rare binucleated cells and micronuclei, and moderate anisocytosis, anisokaryosis, and anisonucleoleosis were noted. The cytologic interpretation was adrenal neoplasia, consistent with adrenal carcinoma. Approximately 4 months later, the cat developed vomiting, dehydration, weakness, and cervical ventroflexion. Serum biochemical alterations at that time included marked hypokalemia (2.4 mmol/L, reference interval 3.4–5.6 mmol/L) and a markedly increased Na:K ratio (65, reference interval 32–41). Mean systolic blood pressure was 205 mmHg. Surgical removal of the mass was accomplished via right adrenalectomy and a diagnosis of adrenal carcinoma was confirmed histologically. Plasma aldosterone concentration (measured preoperatively) was 1358 pmol/L (reference interval 194–388 pmol/L). Primary hyperaldosteronism caused by a functional adrenal carcinoma is an uncommon condition in cats.}, number={1}, journal={VETERINARY CLINICAL PATHOLOGY}, author={Renschler, Janelle S. and Dean, Gregg A.}, year={2009}, month={Mar}, pages={69–72} }
 @article{dean_2008, title={Acute HIV-1 infection: targeting the regulator}, volume={112}, ISSN={["0006-4971"]}, DOI={10.1182/blood-2008-07-165704}, abstractNote={In this issue of Blood , Jiang and colleagues describe the use of humanized rag2-/-γC-/- mice to demonstrate the preferential infection and depletion of Tregs during acute HIV-1 infection.

The role of regulatory T cells (Tregs), phenotypically defined as CD4+CD25+FoxP3+, has been the subject of}, number={7}, journal={BLOOD}, author={Dean, Gregg}, year={2008}, month={Oct}, pages={2600–2600} }
 @article{lankford_petty_la voy_reckling_tompkins_dean_2008, title={Cloning of feline FOXP3 and detection of expression in CD4+CD25+ regulatory T cells}, volume={122}, ISSN={["1873-2534"]}, DOI={10.1016/j.vetimm.2007.11.007}, abstractNote={Regulatory T cells (Treg) are increased and directly infected by feline immunodeficiency virus (FIV) and likely play a role in other feline autoimmune, neoplastic, and infectious diseases. Phenotypically, Treg are best characterized by surface expression of CD4 and CD25 and intranuclear expression of the forkhead transcription factor Foxp3. Our objective was to clone and sequence feline FOXP3 for the purpose of developing assays to enhance studies of feline Treg. We determined the feline FOXP3 is 1293 nucleotides in length and codes for a protein that shares high homology to other species. A splice variant devoid of exon 2 was also identified. A real-time PCR assay was developed and used to show Foxp3 mRNA expression occurs primarily in CD4+CD25+ T cells. Two cross-reacting antibodies were identified by immunocytochemical staining of HEK293 cells transfected with feline FOXP3. The antibody labeling confirmed the nuclear localization of the protein. A flow cytometric assay was also validated and used to correlate the phenotypic and functional characteristics of feline Treg induced by treatment of lymph node lymphocytes with flagellin or LPS in combination with mitogen or IL2. Together, these studies provide useful tools to further investigate Foxp3 and Tregs in cats.}, number={1-2}, journal={VETERINARY IMMUNOLOGY AND IMMUNOPATHOLOGY}, author={Lankford, Susan and Petty, Christopher and La Voy, Alora and Reckling, Stacie and Tompkins, Wayne and Dean, Gregg A.}, year={2008}, month={Mar}, pages={159–166} }
 @article{smithberg_fogle_mexas_reckling_lankford_tompkins_dean_2008, title={In vivo depletion of CD4(+)CD25(+) regulatory T cells in cats}, volume={329}, ISSN={["0022-1759"]}, DOI={10.1016/j.jim.2007.09.015}, abstractNote={To establish a characterized model of regulatory T cell (Treg) depletion in the cat we assessed the kinetics of depletion and rebound in peripheral and central lymphoid compartments after treatment with anti-CD25 antibody as determined by cell surface markers and FOXP3 mRNA expression. An 82% decrease in circulating CD4+CD25+ Tregs was observed by day 11 after treatment. CD4+CD25+ cells were also reduced in the thymus (69%), secondary lymphoid tissues (66%), and gut (67%). Although CD4+CD25+ cells rebound by day 35 post-treatment, FOXP3 levels remain depressed suggesting anti-CD25 antibody treatment has a sustainable diminutive effect on the Treg population. To determine whether CD25+ Treg depletion strategies also deplete activated CD25+ effector cells, cats were immunized with feline immunodeficiency virus (FIV) p24-GST recombinant protein, allowing them to develop a measurable memory response, prior to depletion with anti-CD25 antibody. Anti-FIV p24-GST effector cell activity in peripheral blood after depletion was sustained as determined by antigen-specific T cell proliferation and humoral responses against FIV p24-GST with an ELISA for antigen-specific feline IgG. Furthermore, development of an anti-mouse response in Treg-depleted cats was similar to control levels indicating the retained capacity to respond to a novel antigen. We conclude that despite alterations in CD25+ cell levels during depletion, the feline immune system remains functional. We demonstrate here a model for the study of disease pathogenesis in the context of reduced numbers of immunosuppressive CD4+CD25+ Tregs throughout the feline immune system.}, number={1-2}, journal={JOURNAL OF IMMUNOLOGICAL METHODS}, author={Smithberg, S. Rochelle and Fogle, Jonathan E. and Mexas, Angela M. and Reckling, Stacie K. and Lankford, Susan M. and Tompkins, Mary B. and Dean, Gregg A.}, year={2008}, month={Jan}, pages={81–91} }
 @article{nordone_ignacio_su_sempowski_golenbock_li_dean_2007, title={Failure of TLR4-driven NF-kappa B activation to stimulate virus replication in models of HIV type 1 activation}, volume={23}, ISSN={["0889-2229"]}, DOI={10.1089/aid.2007.0033}, abstractNote={The interaction of HIV-1 with Toll-like receptors (TLR) on host target cells is incompletely understood. Data from several in vivo and in vitro model systems suggest that TLR2, TLR4, and TLR9 remain functional and if stimulated, cause an upregulation of viral replication. In the present studies employing two different chronically HIV-1-infected cell lines and highly purified TLR agonists, we found ligation of TLR2 and TLR9, but not TLR4, resulted in significant upregulation of HIV-1 production. This result was not due to a lack of TLR4 expression or impaired NF-kappa B activation. Using HEK293 cells transfected with individual TLRs and an HIV-1 LTR reporter confirmed that TLR4 signaling does not directly activate the HIV-1 LTR. Finally, ultrapurified LPS did not enhance production of IL-1 beta or IL-6 in chronically infected U1 cells, whereas significant cytokine production was observed in uninfected U937 cells. These results confirm the biological activity of ultrapurified LPS and raise the possibility that TLR4 signaling pathways may be altered during chronic HIV-1 infection. Collectively, these studies suggest that although several TLR can upregulate NF-kappaB in HIV-1-infected cells, upregulation of NF-kappaB alone is insufficient to activate the viral LTR. Further dissection of the TLR signaling pathways is necessary to determine how TLR stimulation leads to LTR activation and whether HIV-1 infection can alter signaling through TLR4.}, number={11}, journal={AIDS RESEARCH AND HUMAN RETROVIRUSES}, author={Nordone, Sushila K. and Ignacio, Glicerio A. and Su, Lishan and Sempowski, Gregory D. and Golenbock, Douglas T. and Li, Liwu and Dean, Gregg A.}, year={2007}, month={Nov}, pages={1387–1395} }
 @article{yearley_stanton_olivry_dean_2007, title={Phagocytic plasmacytoma in a dog}, volume={36}, ISSN={["0275-6382"]}, url={http://www.scopus.com/inward/record.url?eid=2-s2.0-36048964872&partnerID=MN8TOARS}, DOI={10.1111/j.1939-165X.2007.tb00228.x}, abstractNote={Abstract A 4‐year‐old neutered male Golden Retriever was presented to the oncology service of the North Carolina State University Veterinary Teaching Hospital for staging of a histiocytic sarcoma of the left forelimb, diagnosed on the basis of biopsies submitted by the referring veterinarian. Cytologic assessment of aspirates of 2 splenic nodules identified on ultrasonographic examination of the abdomen revealed a highly phagocytic population of neoplastic round cells morphologically suggestive of plasma cells. Histologic assessment of the forelimb mass after amputation of the limb revealed a neoplastic round cell population demonstrating extensive cytophagia and erythrophagia. Immunohistochemical analysis of the tumor population revealed it to be negative for BLA.36 with sporadic positivity for lysozyme and CD79a. Immunofluorescent evaluation revealed weak tumor cell positivity for immunoglobulin (Ig) A and IgM, but extensive strong positivity for IgG, confirming the plasma cell origin of the tumor. Although extensive phagocytic activity may strongly suggest histiocytic origin, plasma cell origin must also be considered among the differential diagnoses for phagocytic round cell tumors.}, number={3}, journal={VETERINARY CLINICAL PATHOLOGY}, author={Yearley, Jennifer H. and Stanton, Christine and Olivry, Thierry and Dean, Gregg A.}, year={2007}, month={Sep}, pages={293–296} }
 @article{gupta_leutenegger_dean_steckbeck_cole_sparger_2007, title={Vaccination of cats with attenuated feline immunodeficiency virus proviral DNA vaccine expressing gamma interferon}, volume={81}, ISSN={["1098-5514"]}, DOI={10.1128/JVI.00815-06}, abstractNote={ABSTRACT}, number={2}, journal={JOURNAL OF VIROLOGY}, author={Gupta, Soumi and Leutenegger, Christian M. and Dean, Gregg A. and Steckbeck, Jonathan D. and Cole, Kelly Stefano and Sparger, Ellen E.}, year={2007}, month={Jan}, pages={465–473} }
 @article{gupta_leutenegger_dean_sparger_2006, title={Construction and characterization of feline immunodeficiency virus proviral mutants that coexpress interferon gamma and green fluorescent protein}, volume={22}, ISSN={["1931-8405"]}, DOI={10.1089/aid.2006.22.342}, abstractNote={Vif deletion mutants of the feline immunodeficiency virus (FIV) were designed to express either enhanced green fluorescent protein (EGFP) (FIVdeltavifATGgfp) or feline interferon-gamma (IFN-gamma) (FIVdeltavifATGgamma) by insertion of the nonviral gene into the deletion site of the viral vif gene. Two in-frame start codons within vif were mutated without altering the overlapping pol translation frame to enhance expression of inserted genes. Expression of EGFP and IFN-gamma from FIVdeltavifATGgfp and FIVdeltavifATGgamma proviruses, respectively, was confirmed by fluorescent microscopy and immunocytochemical assays, respectively. Replication of viruses generated from these proviruses was detectable but severely restricted when compared to that of wild-type (WT) FIV-pPPR. A previous study demonstrated induction of protection against homologous FIV challenge by vaccination of cats with an attenuated FIV-pPPRdeltavif proviral DNA vaccine (Lockridge K et al.: Virology 2000;273:67-79). Coexpression of IFN-gamma or other cytokines from this attenuated provirus provides the opportunity to evaluate the ability of an immunomodulator to enhance the safety and efficacy of an infectious attenuated DNA vaccine. Moreover, a vif-deleted FIV provirus that coexpresses a reporter gene such as EGFP may be used to examine the localization of vif mutant viruses in vivo.}, number={4}, journal={AIDS RESEARCH AND HUMAN RETROVIRUSES}, author={Gupta, S and Leutenegger, C and Dean, G and Sparger, E}, year={2006}, month={Apr}, pages={342–349} }
 @article{dean_lavoy_yearley_stanton_2006, title={Cytokine modulation of the innate immune response in feline immunodeficiency virus - Infected cats}, volume={193}, ISSN={["0022-1899"]}, DOI={10.1086/503873}, abstractNote={BACKGROUND
In vitro data suggest that innate immune function in human immunodeficiency virus type 1-infected patients is compromised; however, in vivo studies are lacking. Feline immunodeficiency virus (FIV) infection in cats provides an excellent model to explore innate immune function in vivo. The innate response against Listeria monocytogenes is well understood, making it a useful immune probe.


METHODS
Recombinant L. monocytogenes carrying eukaryotic expression plasmids for feline tumor necrosis factor (TNF)- alpha , interleukin (IL)-10, interferon (IFN)- gamma , and IL-15 were created to determine whether specific cytokines would modulate innate immune function. L. monocytogenes was delivered subcutaneously, and local lymph nodes were evaluated for size, cell subpopulations, and L. monocytogenes burden. Two months later, memory responses were evaluated by IFN- gamma enzyme-linked immunospot assay.


RESULTS
FIV-positive cats had significantly less lymph-node enlargement and a greater L. monocytogenes burden than FIV-negative control cats. TNF- alpha improved listericidal activity in FIV-negative control cats but not in FIV-positive cats, whereas IL-10 modestly reduced function in FIV-negative control cats. IFN- gamma improved memory responses but not clearance of L. monocytogenes. IL-15 improved innate function in FIV-positive cats and increased the percentage of natural killer cells.


CONCLUSIONS
Lentivirus infection impairs innate immune function in vivo, and IL-15 can significantly restore function. We hypothesize that altered dendritic-cell function and increased regulatory T cell activity may underlie the innate immune defect in HIV infection.}, number={11}, journal={JOURNAL OF INFECTIOUS DISEASES}, author={Dean, GA and Lavoy, A and Yearley, J and Stanton, C}, year={2006}, month={Jun}, pages={1520–1527} }
 @article{olivry_lavoy_dunston_brown_lennon_warren_prisayanh_müller_suter_dean_et al._2006, title={Desmoglein-1 is a minor autoantigen in dogs with pemphigus foliaceus}, volume={110}, ISSN={["0165-2427"]}, url={http://www.scopus.com/inward/record.url?eid=2-s2.0-33644524373&partnerID=MN8TOARS}, DOI={10.1016/j.vetimm.2005.10.002}, abstractNote={The majority of human patients with pemphigus foliaceus (PF) have circulating IgG autoantibodies that target conformational epitopes on the desmosomal cadherin desmoglein-1 (dsg1). Limited studies using immunoblot techniques suggested that the principal autoantigen in dogs with PF might also be dsg1. It was the objective of this study to test this hypothesis. A comprehensive survey of canine PF sera was conducted using a novel screening strategy that detects conformational epitopes. This method consists of the ectopic expression of canine dsg1 at the surface of human 293T epithelial kidney cells and their live screening, i.e. prior to fixation. Out of seven control human PF sera that bound to canine epidermis, three (57%) contained IgG autoantibodies that recognized ectopically expressed canine dsg1 with a membrane and punctate pattern. Out of 83 canine PF sera only five (6%) contained IgG that recognized canine dsg1. Consistent with findings for human PF sera obtained in this study, autoantibody binding was conformation- and glycosylation-dependent as demonstrated by calcium chelation with EDTA and tunicamycin or wheat germ agglutinin treatment, respectively. In conclusion, these studies establish canine dsg1 as a minor autoantigen for canine PF. Antigenic epitopes appear to be conformation- and glycosylation-dependent.}, number={3-4}, journal={VETERINARY IMMUNOLOGY AND IMMUNOPATHOLOGY}, author={Olivry, T. and LaVoy, A. and Dunston, S.M. and Brown, R.S. and Lennon, E.M. and Warren, S.J. and Prisayanh, P. and Müller, E.J. and Suter, M.M. and Dean, G.A. and et al.}, year={2006}, month={Apr}, pages={245–255} }
 @article{dean_barger_lavoy_2005, title={Cloning and expression of feline interleukin 15}, volume={29}, ISSN={["1096-0023"]}, DOI={10.1016/j.cyto.2004.09.012}, abstractNote={A cDNA encoding feline interleukin 15 (IL15) was cloned from the lymph node of a cat infected with feline infectious peritonitis virus. The cDNA is 486 bp in length and encodes a protein of 162 amino acids. Recombinant protein was readily expressed as a GST fusion in Escherichia coli and purified by glutathione affinity chromatography. Expression of recombinant protein in mammalian cells was only accomplished by eliminating the 5′ and 3′ UTR, replacing the IL15 signal peptide with the tissue plasminogen activator signal peptide, and adding 3′ sequence to disrupt presumptive secondary structure of the mRNA. Biologically active feline IL15 was expressed in HEK293T cells and was shown to sustain primary feline lymphocytes, a feline T cell line, and mouse CTLL-2 cells. Proliferation of CTLL-2 cells was induced by the recombinant protein in a dose-dependent manner. Monoclonal and polyclonal antibodies against human IL15 recognized feline IL15 in immunofluorescence and Western blot assays. Additionally, feline IL15 was detectable using a commercially available human IL15 ELISA kit.}, number={2}, journal={CYTOKINE}, author={Dean, GA and Barger, A and LaVoy, A}, year={2005}, month={Jan}, pages={77–83} }
 @article{howard_fisher_dean_burkhard_2005, title={Methodology for isolation and phenotypic characterization of feline small intestinal leukocytes}, volume={302}, ISSN={["1872-7905"]}, DOI={10.1016/j.jim.2005.04.019}, abstractNote={Critical assessment of intestinal immune responses requires the ability to characterize leukocytes from different anatomic locations as leukocytes from inductive sites such as Peyer's patches and lymphoid follicles vary significantly from their effector counterparts, intraepithelial lymphocytes (IEL) and lamina propria lymphocytes (LPL). This study describes (1) methods developed to isolate specific intestinal leukocyte populations with high yield and purity, (2) difficulties encountered in establishing a panel of monoclonal antibodies to assess phenotype, and (3) the phenotypic characterization of effector and inductive sites in the feline small intestine. We found that the phenotypic distribution of feline intestinal leukocytes was similar to that found in other species such as humans, macaques and mice. The majority of IEL were CD5(+) T-cells with less than 7% B-cells. CD8(+) T-cells comprised approximately 60% of the IEL with roughly half displaying CD8alphaalpha homodimers. Approximately 10% of IEL were CD4(+) T-cells. In the LPL, CD4(+) T-cells predominated at 42%, with 33% CD8(+) T-cells and 10% B-cells. As would be expected, B-cells predominated in Peyer's patches with 40% B-cells, 28% CD4(+) T-cells and 20% CD8(+) T-cells. Increased MHCII expression was found in the Peyer's patches as compared to the IEL and LPL. B7.1 expression was significantly higher in mucosal leukocyte populations as compared to organized lymphoid tissue in the periphery with expression detected on 65% of IEL and 53% of LPL. Plasma cells were found in all regions of small intestine examined with greater numbers in lamina propria and Peyer's patches. Lymphoblasts were only identified in inductive tissue. In general, no differences were found between the phenotype of mucosal leukocyte populations from specific pathogen free or random source cats. However, the percentage of CD4(+) CD25(+) T-cells was significantly greater in both IEL and LPL from random source animals. This study provides techniques and a baseline from which future studies of the feline intestinal immune system can be conducted.}, number={1-2}, journal={JOURNAL OF IMMUNOLOGICAL METHODS}, author={Howard, KE and Fisher, IL and Dean, GA and Burkhard, MJ}, year={2005}, month={Jul}, pages={36–53} }
 @article{stevens_lavoy_nordone_burkhard_dean_2005, title={Pre-existing immunity to pathogenic Listeria monocytogenes does not prevent induction of immune responses to feline immunodeficiency virus by a novel recombinant Listeria monocytogenes vaccine}, volume={23}, ISSN={["1873-2518"]}, DOI={10.1016/j.vaccine.2004.09.033}, abstractNote={Listeria monocytogenes is an attractive biologic vaccine vector against HIV because it induces a strong cell mediated immune response, can be delivered by mucosal routes, can be readily manipulated to express viral antigens, and is easy and inexpensive to produce. Proof of concept studies have been performed using HIV Gag expressing recombinant L. monocytogenes in the mouse. Here we report the development and validation of recombinant L. monocytogenes to be evaluated in the FIV/cat model of HIV. Using a simplified approach to introduce individual and polyprotein FIV gag genes, we show that recombinant L. monocytogenes containing the entire gag expresses the full-length Gag polyprotein in a soluble secreted form. A DNA vaccine plasmid (pND14-Lc-env) that replicates in Gram positive bacteria and contains the FIV SU (gp100) and the ectodomain of TM (gp40) in a eukaryotic expression cassette was transfected into LM-gag to create LM-gag/pND14-Lc-env. After infection of target cells with LM-gag/pND14-Lc-env in vitro, both FIV Gag and Env proteins were detected in soluble cell lysates. Whether previous exposure to L. monocytogenes affects the immunogenicity of LM-gag/pND14-Lc-env was determined in cats infected with wild-type L. monocytogenes orally and/or subcutaneously. After a single oral dose of LM-gag/pND14-Lc-env, cats with existing anti-L. monocytogenes immune responses developed anti-FIV Gag IgA titers in vaginal secretions, saliva, and feces. Similarly, FIV Gag and Env specific IFN-γ ELISPOT responses were measurable in spleen and lymph node but at a statistically higher frequency in cats exposed to a single subcutaneous dose of wild-type L. monocytogenes versus cats exposed both subcutaneously and orally. The FIV/cat model will provide a useful challenge system to determine whether recombinant L. monocytogenes can protect against a lentivirus in its natural host after challenge by the routes common to HIV transmission.}, number={12}, journal={VACCINE}, author={Stevens, R and LaVoy, A and Nordone, S and Burkhard, M and Dean, GA}, year={2005}, month={Feb}, pages={1479–1490} }
 @article{ignacio_nordone_howard_dean_2005, title={Toll-like receptor expression in feline lymphoid tissues}, volume={106}, ISSN={["1873-2534"]}, DOI={10.1016/j.vetimm.2005.02.022}, abstractNote={Toll-like receptors (TLRs) are germline-encoded pattern recognition receptors (PRRs) that activate the innate immune system. While it is clear that TLRs are important in the immune response against pathogens, they may also be exploited by some pathogens. Our objective is to determine whether feline immunodeficiency virus (FIV) infection affects TLR expression or function thereby resulting in innate immune dysfunction. To this end, we cloned partial sequences for feline TLRs 1–3, 5–8, and developed real-time PCR assays to quantify feline TLRs 1–9. TLR expression was quantified in normal cat lymphoid tissues, purified lymphocyte subsets, and FIV-infected cell lines. Different expression patterns of TLRs were found in spleen, mesenteric lymph node, retropharyngeal lymph node, thymus, intestinal intraepithelial lymphocytes, and lamina propria lymphocytes. B lymphocytes, CD4+ T cells, and CD8+ T cells all expressed TLRs 2–5, 7–9; however, the relative levels of expression varied among lymphocyte phenotypes. Infection of cell lines with FIV resulted in altered TLR expression levels that differed depending on cell type. These results demonstrate that tissue distribution of TLRs is associated with the immunological role of a particular tissue, that lymphocytes may also express these ‘innate immune’ receptors, and that FIV infection can alter TLR expression.}, number={3-4}, journal={VETERINARY IMMUNOLOGY AND IMMUNOPATHOLOGY}, author={Ignacio, G and Nordone, S and Howard, KE and Dean, GA}, year={2005}, month={Jul}, pages={229–237} }
 @article{sirriyah_dean_lavoy_burkhard_2004, title={Assessment of CD4+ and CD8+ IFN-gamma producing cells by ELISPOT in naive and FIV-infected cats}, volume={102}, ISSN={["1873-2534"]}, DOI={10.1016/j.vetimm.2004.06.011}, abstractNote={IFN-gamma is critical for the development of antiviral cell-mediated immunity in HIV infected humans and FIV infected cats. The ELISPOT has proven to be a technically straightforward assay to quantify the number of IFN-gamma producing cells and offers a reasonable alternative for the quantitative measurement of T-cell function in cats. We used a feline-specific ELISPOT to identify constitutive as well as Con A stimulated IFN-gamma production in T-cell subsets and determine if there were differences between purified (positively sorted) and negatively depleted populations from naïve and FIV infected cats. We found no difference in the total number of PBMC constitutively producing IFN-gamma in naïve and FIV+ cats. Con A exposure was associated with increased numbers of IFN-gamma producing PBMC in naïve, but not FIV+, cats. Equivalent numbers of CD4+ and CD8+ T cells constitutively expressed IFN-gamma in naïve cats. However, in FIV+ cats, the number of IFN-gamma producing CD8+ T-cells was approximately two-fold over that seen for CD4+ T-cells. We found minimal differences between purified (e.g. CD4+ or CD8+) and corresponding depleted (e.g. CD8- or CD4-) populations in samples from FIV+ cats. In contrast, depleted populations from naïve cats showed greater response to Con A than did purified populations. Thus, while determination of the number of IFN-gamma producing cells by feline-specific ELISPOT is a useful tool for the evaluation of the feline immune response, determination of the initial sample population and T-cell subset is critical for optimal interpretation of the IFN-gamma ELISPOT.}, number={1-2}, journal={VETERINARY IMMUNOLOGY AND IMMUNOPATHOLOGY}, author={Sirriyah, J and Dean, GA and LaVoy, A and Burkhard, MJ}, year={2004}, month={Nov}, pages={77–84} }
 @article{stevens_howard_nordone_burkhard_dean_2004, title={Oral immunization with recombinant Listeria monocytogenes controls virus load after vaginal challenge with feline immunodeficiency virus}, volume={78}, ISSN={["1098-5514"]}, DOI={10.1128/JVI.78.15.8210-8218.2004}, abstractNote={ABSTRACT}, number={15}, journal={JOURNAL OF VIROLOGY}, author={Stevens, R and Howard, KE and Nordone, S and Burkhard, M and Dean, GA}, year={2004}, month={Aug}, pages={8210–8218} }
 @article{dean_lavoy_burkhard_2004, title={Peptide mapping of feline immunodeficiency virus by IFN-gamma elispot}, volume={100}, ISSN={["1873-2534"]}, DOI={10.1016/j.vetimm.2004.03.001}, abstractNote={Interferon-gamma (IFN-γ) enzyme-linked immunospot (ELISPOT) has become an important tool in studying antigen-specific T lymphocyte responses. Soluble peptides can be used to map T-cell epitopes, providing information that is useful in the design and evaluation of vaccines as well as studies of immunopathogenesis. To date, this assay has not been widely utilized in feline immunodeficiency virus (FIV) research. We have developed a feline IFN-γ ELISPOT assay and used it to determine FIV-specific T-cell epitopes recognized by infected cats. A panel of 331 peptides, 15 amino acids in length and overlapping by 10 residues was synthesized. The peptide library spanned the FIV structural (Gag), envelope (Env), reverse transcriptase (RT), and open-reading-frame A (OrfA) proteins. Initially, 34 pools, containing 7–10 peptides each were screened by IFN-γ ELISPOT against peripheral blood mononuclear cells (PBMC) from eight cats chronically infected with the NCSU1 molecular clone of FIV and four uninfected control cats. Individual peptides from pools recognized by FIV+ cats were then evaluated and optimal peptides were combined into pools representing Gag, Env, RT, and OrfA. A higher percentage of FIV infected cats were identified as responders against the peptide pools when using fresh PBMC as compared to cryopreserved PBMC. In vitro restimulation of cryopreserved PBMC with the peptide pools improved the sensitivity of the assay to similar levels as observed from fresh samples. Individual peptides used in the pools were generally found to stimulate CD8+ T-cells more efficiently than CD4+ T-cells. Comparison of the peptide sequences to representative FIV sequences from clades A–D showed conservation was high among Gag and RT peptides, variable among Env peptides and low for OrfA peptides. The IFN-γ ELISPOT assay and FIV-specific peptide pools we describe here will be useful in assessing cell-mediated responses to experimental FIV vaccines.}, number={1-2}, journal={VETERINARY IMMUNOLOGY AND IMMUNOPATHOLOGY}, author={Dean, GA and LaVoy, A and Burkhard, MJ}, year={2004}, month={Jul}, pages={49–59} }
 @article{olivry_dunston_rivierre_jackson_murphy_peters_dean_2003, title={A randomized controlled trial of misoprostol monotherapy for canine atopic dermatitis: effects on dermal cellularity and cutaneous tumour necrosis factor-alpha}, volume={14}, ISSN={["0959-4493"]}, url={http://www.scopus.com/inward/record.url?eid=2-s2.0-0037310297&partnerID=MN8TOARS}, DOI={10.1046/j.1365-3164.2003.00323.x}, abstractNote={Abstract In this blinded randomized placebo‐controlled trial, 20 dogs with atopic dermatitis (AD) were given placebo (8 dogs) or misoprostol (12 dogs) at 5 µg kg−1, orally, three times daily for 3 weeks. Administration of the active drug, but not of placebo, led to a significant decrease in lesional and pruritus scores. The median reduction from baseline of both scores was ≈30%. Misoprostol therapy did not lead to decreases of dermal cell counts or skin tumour necrosis factor (TNF)α mRNA copy numbers that were significantly different from those of placebo. Skin TNFα protein production, assessed using indirect immunofluorescence, decreased or remained unchanged in dogs receiving misoprostol. In contrast, post treatment TNFα fluorescence scores were higher in all but two dogs given placebo. The changes from baseline of TNFα fluorescence scores did not correlate significantly with those of lesional or pruritus indices. These observations confirm the modest efficacy of misoprostol for treatment of canine AD and suggest that its mild anti‐allergic effects are not associated with either inhibition of inflammatory cell emigration or TNFα production.}, number={1}, journal={VETERINARY DERMATOLOGY}, author={Olivry, T and Dunston, SM and Rivierre, C and Jackson, HA and Murphy, KM and Peters, E and Dean, GA}, year={2003}, month={Feb}, pages={37–46} }
 @article{dean_olivry_stanton_pedersen_2003, title={In vivo cytokine response to experimental feline infectious peritonitis virus infection}, volume={97}, ISSN={["0378-1135"]}, url={http://www.scopus.com/inward/record.url?eid=2-s2.0-0344154638&partnerID=MN8TOARS}, DOI={10.1016/j.vetmic.2003.08.010}, abstractNote={Feline infectious peritonitis virus (FIPV) is a coronavirus that causes sporadic fatal disease in cats characterized by vasculitis, granulomatous inflammation and effusive pleuritis/peritonitis. Histologic changes in lymphoid tissues include lymphoid hyperplasia, lymphoid depletion, histiocytosis, and granuloma formation. Although viremia occurs, histologic lesions are not found uniformly throughout lymphoid tissues. We used experimental infection of cats with a highly pathogenic FIPV isolate, UCD8, to study histologic lesions, virus replication, and cytokine expression in multiple lymphoid tissues during the effusive phase of disease. Viral RNA was found in 76% of central tissues (mediastinal lymph node, spleen, mesenteric lymph node) examined, as compared to 27% of peripheral tissues (popliteal lymph node, cervical lymph node, femoral bone marrow). All tissues positive for virus replication also demonstrated lymphoid depletion. Generally, affected tissues had lower levels of IL-4 and IL-12–p40 mRNA and higher levels of IL-10 mRNA. Although no differences in IFN-γ or TNF-α mRNA were measured, TNF-α protein expression was greater in affected tissues and demonstrated a shift in the source of TNF-α from macrophages to lymphocytes. Together, these results colocalize FIPV replication, lymphocyte depletion in tissues, and alterations in cytokine transcription and translation. A possible role for TNF-α in the previously described FIPV-induced lymphocyte apoptosis is also suggested.}, number={1-2}, journal={VETERINARY MICROBIOLOGY}, author={Dean, GA and Olivry, T and Stanton, C and Pedersen, NC}, year={2003}, month={Dec}, pages={1–12} }
 @misc{burkhard_dean_2003, title={Transmission and immunopathogenesis of FIV in cats as a model for HIV}, volume={1}, ISSN={["1873-4251"]}, DOI={10.2174/1570162033352101}, abstractNote={The feline immunodeficiency virus (FIV) model provides a system to study lentivirus transmission, virus kinetics, pathogenesis, host responses, and immune dysfunction in a natural, out-bred host, under controlled conditions with specific-pathogen-free animals. The diversity of primary FIV strains can be exploited to mirror the range of disease manifestations associated with HIV infection. FIV is infectious via intravenous, intraperitoneal, intradermal, or subcutaneous injection as well as by atraumatic instillation onto the oral, vaginal, or rectal mucosa. Together, these features allow investigators to model specific aspects of HIV infection in a highly relevant and relatively inexpensive animal model. Well-developed areas of the FIV model include: (1) transmission of cell-associated as well as cell-free virus; (2) mucosal infectivity and immunopathogenesis; (3) vertical transmission; (4) acquired immunodeficiency including defects of the innate immune system; (5) thymic dysfunction; (6) neurotropism and neuropathogenesis; (7) host-virus interactions and the role of specific gene products; (8) efficacy of antiviral therapy; and (9) efficacy and immune correlates of experimental vaccines. This review will encompass areas specific to transmission and immunopathogenesis.}, number={1}, journal={CURRENT HIV RESEARCH}, author={Burkhard, MJ and Dean, GA}, year={2003}, month={Jan}, pages={15–29} }
 @article{burkhard_valenski_leavell_dean_tompkins_2002, title={Evaluation of FIV protein-expressing VEE-replicon vaccine vectors in cats}, volume={21}, ISSN={["0264-410X"]}, DOI={10.1016/S0264-410X(02)00455-3}, abstractNote={Venezuelan equine encephalitis (VEE) virus-replicon particles (VRP) were used to generate feline immunodeficiency virus (FIV) Gag- and ENV-expressing vaccine vectors. Serum and mucosal FIV-specific antibody was detected in cats immunized subcutaneously, once monthly for 5 months, with FIV-expressing VRP. Expansion of the CD8+ L-selectin negative phenotype and transient CD8+ noncytolytic suppressor activity were seen in cats immunized with FIV-expressing or control VRP. Despite induction of FIV-specific immune responses and nonspecific suppressor responses, all cats became infected following vaginal challenge with high dose, pathogenic cell-associated FIV-NCSU(1) although relative early maintenance of CD4+ cells was seen in FIV-immunized cats.}, number={3-4}, journal={VACCINE}, author={Burkhard, MJ and Valenski, L and Leavell, S and Dean, GA and Tompkins, WAF}, year={2002}, month={Dec}, pages={258–268} }
 @article{roosje_dean_willemse_rutten_thepen_2002, title={Interleukin 4-producing CD4+ T cells in the skin of cats with allergic dermatitis}, volume={39}, ISSN={["1544-2217"]}, DOI={10.1354/vp.39-2-228}, abstractNote={Lesional skin of cats with allergic dermatitis has a cellular infiltrate and a CD4/CD8 ratio comparable to that in humans with atopic dermatitis. CD4+ helper T cells and in particular cells belonging to the Th2 subset play an important role in disease pathogenesis in humans. We investigated the cytokine pattern of CD4+ T cells in situ, with special emphasis on the putative presence of cells producing interleukin 4 (IL4), in cats with allergic dermatitis. Immunohistochemical procedures were used to determine that CD4+ T cells in lesional and nonlesional skin of cats with allergic dermatitis can produce IL4, as occurs in humans. Lesional and nonlesional skin of cats with allergic dermatitis had significantly more IL4+ T cells ( P = 0.001) than did skin of healthy control cats. Double staining indicated that all IL4+ cells were positive for pan-T or CD4 markers. Double labeling for mast cell chymase and IL4 stained primarily different cells. Western blotting demonstrated cross-reactivity between the antibody against human IL4 and a feline recombinant IL4. These results indicate that IL4 is primarily produced by CD4+ T cells and is also present in clinically uninvolved skin, indicating a role in the pathogenesis of allergic dermatitis in cats.}, number={2}, journal={VETERINARY PATHOLOGY}, author={Roosje, PJ and Dean, GA and Willemse, T and Rutten, VPMG and Thepen, T}, year={2002}, month={Mar}, pages={228–233} }
 @article{neel_dean_2000, title={A mass in the spinal column of a dog}, volume={29}, ISSN={["0275-6382"]}, url={http://www.scopus.com/inward/record.url?eid=2-s2.0-0034391028&partnerID=MN8TOARS}, DOI={10.1111/j.1939-165X.2000.tb00409.x}, abstractNote={Veterinary Clinical PathologyVolume 29, Issue 3 p. 87-89 A Mass in the Spinal Column of a Dog Jennifer Neel DVM, Corresponding Author Jennifer Neel DVM Department of Microbiology, Pathology, and Parasitology, College of Veterinary Medicine, North Carolina State University, Raleigh, NC.Corresponding author: Jennifer Neel, DVM, Department of Microbiology, Pathology, and Parasitology, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough St, Raleigh, NC 27606 (e-mail: [email protected]).Search for more papers by this authorGregg A. Dean DVM, PhD, Gregg A. Dean DVM, PhD Department of Microbiology, Pathology, and Parasitology, College of Veterinary Medicine, North Carolina State University, Raleigh, NC.Search for more papers by this author Jennifer Neel DVM, Corresponding Author Jennifer Neel DVM Department of Microbiology, Pathology, and Parasitology, College of Veterinary Medicine, North Carolina State University, Raleigh, NC.Corresponding author: Jennifer Neel, DVM, Department of Microbiology, Pathology, and Parasitology, College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough St, Raleigh, NC 27606 (e-mail: [email protected]).Search for more papers by this authorGregg A. Dean DVM, PhD, Gregg A. Dean DVM, PhD Department of Microbiology, Pathology, and Parasitology, College of Veterinary Medicine, North Carolina State University, Raleigh, NC.Search for more papers by this author First published: 05 March 2008 https://doi.org/10.1111/j.1939-165X.2000.tb00409.xCitations: 11Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat References 1 Clark DM, Picut CA. Neuroepithelioma in a middle-aged dog. JAVMA. 1986; 189: 1330–1331. CASPubMedWeb of Science®Google Scholar 2 Summers BA, de Lahunta A, McEntee M, Kuhajda FP. A novel intradural extramedullary spinal cord tumor in young dogs. Acta Neuropathol. 1988; 75: 402–410. 10.1007/BF00687794 CASPubMedWeb of Science®Google Scholar 3 Moissonnier P, Abbott D. Canine neuroepithelioma: case report and literature review. JAAHA. 1993; 29: 397–401. Web of Science®Google Scholar 4 Ferretti A, Scanziani E, Colombo S. Surgical treatment of a spinal cord tumor resembling nephroblastoma in a young dog. Prog Vet Neurol. 1993; 4: 84–87. Web of Science®Google Scholar 5 Terrell SF, Platt SR, Chrisman CL. Possible intraspinal metastasis of a canine spinal cord nephroblastoma. Vet Pathol. 2000; 37: 94–97. 10.1354/vp.37-1-94 CASPubMedWeb of Science®Google Scholar 6 Macri NP, Van Alstine W, Coolman RA. Canine spinal nephroblastoma. JAAHA. 1997; 33: 302–306. 10.5326/15473317-33-4-302 CASPubMedWeb of Science®Google Scholar 7 Pearson GR, Gregory SP, Charles AK. Immunohistochemical demonstration of Wilms' tumor gene product WT1 in a canine “neuroepithelioma” providing evidence for its classification as an extrarenal nephroblastoma. J Comp Pathol. 1997; 116: 321–327. 10.1016/S0021-9975(97)80006-0 CASPubMedWeb of Science®Google Scholar 8 Cotran RS, Kumar V, Robbins SL. Robbins Pathologic Basis of Disease. 5th ed. Philadelphia , Pa : WB Saunders; 1994: 464–456. Google Scholar Citing Literature Volume29, Issue3September 2000Pages 87-89 ReferencesRelatedInformation}, number={3}, journal={VETERINARY CLINICAL PATHOLOGY}, author={Neel, J and Dean, GA}, year={2000}, pages={87–89} }
 @article{lockridge_chien_dean_cole_montelaro_luciw_sparger_2000, title={Protective immunity against feline immunodeficiency virus induced by inoculation with vif-deleted proviral DNA}, volume={273}, ISSN={["1089-862X"]}, DOI={10.1006/viro.2000.0395}, abstractNote={To determine whether live-attenuated feline immunodeficiency virus (FIV) proviral DNA will induce protective immunity, a plasmid clone constructed with a FIV provirus containing a deletion in the viral accessory gene vif (FIV-pPPR-Deltavif) was inoculated as proviral DNA into four cats by the intramuscular route. After 43 weeks, these cats were boosted with the same proviral plasmid. Analysis of peripheral blood mononuclear cells at several time points after the primary and booster inoculations revealed no detectable virus or proviral DNA. At 6 weeks after the booster, immunized cats and additional naive control cats were challenged with a cell-free preparation of the infectious biological isolate FIV-PPR by the intraperitoneal route. Virus was detected after challenge in unvaccinated control cats but not in any of the FIV-pPPR-Deltavif-immunized cats. Both FIV Gag- and Env-specific cytotoxic T lymphocyte (CTL) activities were detected in peripheral blood cells of control cats after challenge infection, whereas only one of four cats immunized with FIV-pPPR-Deltavif DNA exhibited a measurable CTL response to Env following challenge. Although anti-Gag antibodies were not detected after both proviral DNA inoculation and challenge, anti-Env antibodies were found in FIV-pPPR-Deltavif-immunized cats after vaccination as well as after challenge. These findings indicate that inoculation with FIV-pPPR-Deltavif proviral DNA induced resistance to challenge with infectious FIV and that a vif deletion mutant may provide a relatively safe attenuated lentiviral vaccine.}, number={1}, journal={VIROLOGY}, author={Lockridge, KM and Chien, M and Dean, GA and Cole, KS and Montelaro, RC and Luciw, PA and Sparger, EE}, year={2000}, month={Jul}, pages={67–79} }
 @article{dean_himathongkham_sparger_1999, title={Differential cell tropism of feline immunodeficiency virus molecular clones in vivo}, volume={73}, number={4}, journal={Journal of Virology}, author={Dean, G. A. and Himathongkham, S. and Sparger, E. E.}, year={1999}, pages={2596–2603} }
 @article{woo_dean_lavoy_clark_moore_1999, title={Investigation of recombinant human insulin-like growth factor type I in thymus regeneration in the acute stage of experimental FIV infection in juvenile cats}, volume={15}, ISSN={["1931-8405"]}, DOI={10.1089/088922299310089}, abstractNote={Thymus involvement and the development of thymic lesions in HIV-1 infection is hypothesized to suppress thymus function and limit T cell maturation and replenishment of the peripheral lymphoid pool. Therapeutic modulation to protect or enhance thymus function may therefore ameliorate peripheral lymphocytopenia and retard disease progression. Thymotrophic agents, such as insulin-like growth factor type I (IGF-I), may therefore represent adjunctive but important methods of treatment to protect or promote thymus function. The assessment of rhIGF-I in lentiviral infection and its impact on the thymus was performed using the feline immunodeficiency virus (FIV) model. Regeneration of the thymus in juvenile cats and amelioration of the thymic lesion after FIV infection was assessed by multiple measurements including thymic weight, stereologic analysis of the thymus cortex and medulla, histologic and immunohistologic analysis, quantitation of thymocyte and peripheral lymphocyte subsets, and quantitative competitive RT-PCR. Evidence of thymic cortical regeneration was observed in FIV-inoculated cats after 12 and 20 weeks of rhIGF-I treatment. Inflammation in the thymus was reduced during this period of treatment in this group of rhIGF-I/FIV-inoculated cats as evidenced by the reduced numbers of B cells detected. Viral replication rates in peripheral lymph nodes were not altered by rhIGF-I treatment and were decreased by 1 log in the thymus after 20 weeks of treatment. Peripheral blood CD4+ T cell counts also increased after 14 weeks of treatment. This suggests that rhIGF-I treatment can enhance thymus function and replenishment of the peripheral T cell pool.}, number={15}, journal={AIDS RESEARCH AND HUMAN RETROVIRUSES}, author={Woo, JC and Dean, GA and Lavoy, A and Clark, R and Moore, PF}, year={1999}, month={Oct}, pages={1377–1388} }
 @article{olivry_dean_tompkins_dow_moore_1999, title={Toward a canine model of atopic dermatitis: amplification of cytokine-gene transcripts in the skin of atopic dogs}, volume={8}, ISSN={["0906-6705"]}, DOI={10.1111/j.1600-0625.1999.tb00372.x}, abstractNote={Abstract:  The objectives of the present study were to characterize and compare the repertoire of cytokine‐genes transcribed in skin homogenates obtained from normal dogs and dogs with atopic dermatitis (AD) using a reverse‐transcriptase polymerase chain reaction and canine‐specific cytokine‐gene primers. Whereas IL‐4 and IL‐5 cytokine‐gene transcripts were detected more commonly in atopic skin biopsy homogenates, IL‐2 mRNA was amplified more often from normal control specimens. IFN‐γ mRNA was detected in 5/29 atopic specimens, 4 of them obtained from the only dog with chronic skin lesions. One‐fourth of atopic samples exhibited clear type‐2 cytokine profiles; the remainder did not demonstrate polarized repertoires. Conversely, type‐1 cytokine profiles were characterized in one‐fourth of normal control specimens. The present study establishes, for the first time, the transcription of type‐2 cytokine‐genes in the skin of dogs with AD. Future experiments investigating the cellular origin and dynamics of allergic cytokine‐gene transcription are needed to confirm whether or not canine AD could be considered an immunological model for a human disease.}, number={3}, journal={EXPERIMENTAL DERMATOLOGY}, author={Olivry, T and Dean, GA and Tompkins, MB and Dow, JL and Moore, PF}, year={1999}, month={Jun}, pages={204–211} }
 @article{dean_pedersen_1998, title={Cytokine response in multiple lymphoid tissues during the primary phase of feline immunodeficiency virus infection}, volume={72}, number={12}, journal={Journal of Virology}, author={Dean, G. A. and Pedersen, N. C.}, year={1998}, pages={9436–9440} }
 @article{dean_bernales_pedersen_1998, title={Effect of feline immunodeficiency virus on cytokine response to Listeria monocytogenes in vivo}, volume={65}, ISSN={["1873-2534"]}, DOI={10.1016/S0165-2427(98)00148-2}, abstractNote={Feline immunodeficiency virus (FIV) is a lentivirus that induces an acquired immunodeficiency in domestic cats. The objective of this study was to compare the immune response of chronically FIV-infected cats and specific pathogen free (SPF) cats to Listeria monocytogenes, a facultative intracellular bacterium. Regional lymph nodes were removed at various times after subcutaneous inoculation with L. monocytogenes and evaluated. Lymph nodes of chronically FIV-infected cats enlarged more slowly and to a lesser degree than SPF cats. This was due to delayed and blunted lymphoid follicle formation and markedly diminished histiocyte influx. The cellular response correlated with a marked upregulation in IL10 transcription and delayed increase in TNF-α upregulation in FIV-infected cats. Transcriptional upregulation of IFN-γ, IL4, and the p40 chain of IL12 was similar in lymph nodes of FIV-infected and SPF cats. Clinically, FIV-infected cats had a more severe response at the site of L. monocytogenes injection and showed signs of systemic bacterial dissemination while SPF cats remained clinically normal. FIV-infected cats generated a delayed hypersensitivity response similar to SPF cats but also had a significantly greater antibody response. Taken together, these data suggest excessive IL10 production may be responsible for the deficiency observed in the innate immune response of chronically FIV-infected cats challenged with L. monocytogenes.}, number={2-4}, journal={VETERINARY IMMUNOLOGY AND IMMUNOPATHOLOGY}, author={Dean, GA and Bernales, JA and Pedersen, NC}, year={1998}, month={Oct}, pages={125–138} }
 @article{elder_dean_hoover_hoxie_malim_mathes_neil_north_sparger_tompkins_et al._1998, title={Lessons from the cat: Feline immunodeficiency virus as a tool to develop intervention strategies against human immunodeficiency virus type 1}, volume={14}, ISSN={["0889-2229"]}, DOI={10.1089/aid.1998.14.797}, abstractNote={AIDS Research and Human RetrovirusesVol. 14, No. 9 Workshop Summary: Lessons from the Cat: Feline Immunodeficiency Virus as a Tool to Develop Intervention Strategies against Human Immunodeficiency Virus Type 1JOHN H. ELDER, GREGG A. DEAN, EDWARD A. HOOVER, JAMES A. HOXIE, MICHAEL H. MALIM, LAWRENCE MATHES, JAMES C. NEIL, THOMAS W. NORTH, ELLEN SPARGER, MARY B. TOMPKINS, WAYNE A.F. TOMPKINS, JANET YAMAMOTO, NAOYA YUHKI, NEILS C. PEDERSEN, and ROGER H. MILLERJOHN H. ELDERSearch for more papers by this author, GREGG A. DEANSearch for more papers by this author, EDWARD A. HOOVERSearch for more papers by this author, JAMES A. HOXIESearch for more papers by this author, MICHAEL H. MALIMSearch for more papers by this author, LAWRENCE MATHESSearch for more papers by this author, JAMES C. NEILSearch for more papers by this author, THOMAS W. NORTHSearch for more papers by this author, ELLEN SPARGERSearch for more papers by this author, MARY B. TOMPKINSSearch for more papers by this author, WAYNE A.F. TOMPKINSSearch for more papers by this author, JANET YAMAMOTOSearch for more papers by this author, NAOYA YUHKISearch for more papers by this author, NEILS C. PEDERSENSearch for more papers by this author, and ROGER H. MILLERSearch for more papers by this authorPublished Online:15 Mar 2009https://doi.org/10.1089/aid.1998.14.797AboutSectionsPDF/EPUB ToolsPermissionsDownload CitationsTrack CitationsAdd to favorites Back To Publication ShareShare onFacebookTwitterLinked InRedditEmail FiguresReferencesRelatedDetailsCited ByEqual contributions of feline immunodeficiency virus and coinfections to morbidity in African lionsInternational Journal for Parasitology: Parasites and Wildlife, Vol. 16Pathogenesis of oral FIV infection21 September 2017 | PLOS ONE, Vol. 12, No. 9Structural features of the C8 antiviral peptide in a membrane-mimicking environmentBiochimica et Biophysica Acta (BBA) - Biomembranes, Vol. 1838, No. 3Accessory Genes Confer a High Replication Rate to Virulent Feline Immunodeficiency VirusJournal of Virology, Vol. 87, No. 14In Vivo Assessment of Natural Killer Cell Responses during Chronic Feline Immunodeficiency Virus Infection31 May 2012 | PLoS ONE, Vol. 7, No. 5FIV diversity: FIVPle 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(FIV-Apetaluma and FIV-Cpgammar) in young adult specific pathogen free catsVeterinary Immunology and Immunopathology, Vol. 79, No. 1-2FELINE IMMUNODEFICIENCY VIRUSHuman Immunodeficiency Virus and AIDS: Insights from Animal LentivirusesJournal of Virology, Vol. 74, No. 16Alteration of Substrate and Inhibitor Specificity of Feline Immunodeficiency Virus ProteaseJournal of Virology, Vol. 74, No. 10Structural studies of FIV and HIV-1 proteases complexed with an efficient inhibitor of FIV proteaseProteins: Structure, Function, and Genetics, Vol. 38, No. 1Construction of Infectious Feline Foamy Virus Genomes: Cat Antisera Do Not Cross-Neutralize Feline Foamy Virus Chimera with Serotype-Specific Env SequencesVirology, Vol. 266, No. 1Neurophysiologic and Immunologic Abnormalities Associated With Feline Immunodeficiency Virus Molecular Clone FIV-PPR DNA InoculationJournal of Acquired Immune Deficiency Syndromes, Vol. 23, No. 1Neurophysiologic and Immunologic Abnormalities Associated With Feline Immunodeficiency Virus Molecular Clone FIV-PPR DNA InoculationJAIDS Journal of Acquired Immune Deficiency Syndromes, Vol. 23, No. 1Site-specific Incorporation of Nucleoside Analogs by HIV-1 Reverse Transcriptase and the Template Grip Mutant P157SJournal of Biological Chemistry, Vol. 275, No. 1AIDS vaccination studies using feline immunodeficiency virus as a model: immunisation with inactivated whole virus suppresses viraemia levels following intravaginal challenge with infected cells but not following intravenous challenge with cell-free virusVaccine, Vol. 18, No. 1-2Cyanovirin-N Binds to gp120 To Interfere with CD4-Dependent Human Immunodeficiency Virus Type 1 Virion Binding, Fusion, and Infectivity but Does Not Affect the CD4 Binding Site on gp120 or Soluble CD4-Induced Conformational Changes in gp120Journal of Virology, Vol. 73, No. 5 Volume 14Issue 9Jun 1998 To cite this article:JOHN H. ELDER, GREGG A. DEAN, EDWARD A. HOOVER, JAMES A. HOXIE, MICHAEL H. MALIM, LAWRENCE MATHES, JAMES C. NEIL, THOMAS W. NORTH, ELLEN SPARGER, MARY B. TOMPKINS, WAYNE A.F. TOMPKINS, JANET YAMAMOTO, NAOYA YUHKI, NEILS C. PEDERSEN, and ROGER H. MILLER.Workshop Summary: Lessons from the Cat: Feline Immunodeficiency Virus as a Tool to Develop Intervention Strategies against Human Immunodeficiency Virus Type 1.AIDS Research and Human Retroviruses.Jun 1998.797-801.http://doi.org/10.1089/aid.1998.14.797Published in Volume: 14 Issue 9: March 15, 2009PDF download}, number={9}, journal={AIDS RESEARCH AND HUMAN RETROVIRUSES}, author={Elder, JH and Dean, GA and Hoover, EA and Hoxie, JA and Malim, MH and Mathes, L and Neil, JC and North, TW and Sparger, E and Tompkins, MB and et al.}, year={1998}, month={Jun}, pages={797–801} }
 @article{pedersen_dean_bernales_sukura_higgins_1998, title={Listeria monocytogenes and Serratia marcescens infections as models for Th1/Th2 immunity in laboratory cats}, volume={63}, ISSN={["1873-2534"]}, DOI={10.1016/S0165-2427(98)00085-3}, abstractNote={Five species of bacteria known to be naturally-occurring pathogens of cats were screened for their ability to grow in feline macrophages in vitro, and to induce antibodies and delayed type hypersensitivity (DTH) responses in vivo. Two of these organisms, L. monocytogenes and S. marcescens, were selected for further study based on clear-cut differences in their in vitro and in vivo behavior. Listeria was macrophage tropic, induced DTH, and evoked poor antibody responses post-recovery, whereas Serratia remained extracellular, did not induce a DTH reaction, and produced high titer of antibodies. Young specific pathogen free cats were then inoculated subcutaneously into the drainage areas of the right and left popliteal and auricular lymph nodes with either L. monocytogenes or S. marcescens. Each of the four lymph nodes were then removed in sequence over a two week period, weighed, cultured for viable bacteria, and RNA extracted for Th1/Th2 cytokine mRNA quantitation. Antibody responses and delayed type hypersensitivity responses were also measured. Identical to pilot studies, cats infected with Serratia developed very high levels of antibody compared to Listeria infected cats but no DTH, while Listeria infected cats produced negligible or low titers of antibodies and strong DTH. Immunity to Listeria occurred around 168 h post infection as evidenced by the disappearance of living bacteria from the nodes, while immunity to Serratia took over 264 h. Pronounced lymph node hyperplasia occurred in both infections, but persisted longer for Serratia. Enlargement of Serratia infected nodes was associated with marked follicular, primary and secondary germinal center and medullary hyperplasia. Germinal center formation in Listeria stimulated nodes was much less intense and dense accumulations of macrophages dissected between follicles downward from the subcapsular sinuses. Although functional and histologic studies showed a clear-cut cell-mediated vs. humoral response in the respective Listeria and Serratia infections, preferential cytokine mRNA upregulation was observed for only two of the five major Th1/Th2 cytokines measured. Interferon-γ, a Th1 cytokine, was much more elevated in the Listeria stimulated nodes, but TNF-α (also a Th1 cytokine) was more elevated in Serratia infected nodes. Interleukin-12, an important Th1 cytokine, was elevated to equal levels in both infections as were the Th2 cytokines IL-4 and IL-10.}, number={1-2}, journal={VETERINARY IMMUNOLOGY AND IMMUNOPATHOLOGY}, author={Pedersen, NC and Dean, GA and Bernales, J and Sukura, A and Higgins, J}, year={1998}, month={May}, pages={83–103} }
 @article{dean_higgins_lavoy_fan_pedersen_1998, title={Measurement of feline cytokine gene expression by quantitative-competitive RT-PCR}, volume={63}, ISSN={["0165-2427"]}, DOI={10.1016/S0165-2427(98)00084-1}, abstractNote={We have developed a method to quantitate feline cytokine gene expression using competitive RT-PCR. Feline cytokine specific primers were developed that encompass an intron, thus allowing differentiation of cDNA vs. genomic DNA amplification products. The PCR products of the primers were verified by sequencing and Southern blot analysis. For quantitation, a non-homologous RNA competitor was created for each cytokine of interest. The competitor was designed to yield an RT-PCR product 10–20% larger than the native sequence, thereby allowing differentiation of the two products by electrophoresis on an agarose gel. Both competitor and native sequences used the same primer sequences for RT (oligo dT) and PCR (cytokine specific). The amplification efficiency of the competitor and native sequence was shown to be identical which allowed comparison at any point during the amplification, including the plateau phase. The quantity of starting cytokine mRNA was determined by interpolation from a standard curve. As little as 1 μg of total cellular RNA was required per cytokine determination. The assay can routinely quantify as few as 1000 copies of template and spans a range of up to 4 log.}, number={1-2}, journal={VETERINARY IMMUNOLOGY AND IMMUNOPATHOLOGY}, author={Dean, GA and Higgins, J and LaVoy, A and Fan, ZY and Pedersen, NC}, year={1998}, month={May}, pages={73–82} }