@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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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} }
 @article{strahl_huang_pedersen_wu_ghosh_miller_1997, title={Two proximal activating protein-1-binding sites are sufficient to stimulate transcription of the ovine follicle-stimulating hormone-beta gene}, volume={138}, ISSN={["1945-7170"]}, DOI={10.1210/en.138.6.2621}, abstractNote={FSH is an important regulator of mammalian gametogenesis and the female reproductive cycle. Although little is known about the transcriptional regulation of the β-subunit (the rate-limiting subunit of FSH synthesis), sequence analysis of the ovine FSHβ promoter has revealed a number of potential activating protein-1 (AP-1; Jun/Fos)-binding sites. To determine whether the gene encoding theβ -subunit of ovine FSH (oFSHβ) is responsive to AP-1 transcriptional complexes, chimeric constructs containing deleted portions of the oFSHβ promoter fused to a luciferase reporter were transiently transfected along with c-Jun and c-Fos expression constructs into JAR cells. Analysis of these deletion constructs revealed that the proximal promoter of oFSHβ is highly stimulated by c-Jun and c-Fos proteins (typically 20-fold with a reporter construct containing oFSHβ sequences from −215 to +759 bp). This stimulation was lost when a similar construct containing sequences from −84 to+ 759 bp was tested. Transcriptional start site analysis using reverse transcription-PCR verified that the transcriptional initiation of the− 215-bp deletion construct, with or without cotransfected c-Jun/c-Fos, was the same as that observed in vivo. Computer analysis of oFSHβ sequences from −215 to +1 bp identified four putative AP-1-like elements, located at −155, −120, −83, and −10 bp. Gel retardation experiments using oligonucleotides corresponding to the four putative AP-1-like sites revealed that only −120 and −83 sites in oFSHβ bound AP-1 proteins in vitro. Site-directed mutagenesis of the −120 and −83 sites showed that each element was required for stimulation by c-Jun and c-Fos proteins as well as 12-O-tetradecanoyl phorbol-13-acetate in transient transfection assays. Finally, immunocytochemical dual labeling was used to show that more than 75% of all FSHβ-containing cells in ovine pituitary sections from cycling ewes contained nuclear c-Jun, JunB, JunD, and Fos proteins. These data, taken together, show that oFSHβ transcription can be stimulated by c-Jun and c-Fos proteins via two functionally linked AP-1-like sites in the oFSHβ proximal promoter and that these sites are likely to be important regulators of FSH production in vivo.}, number={6}, journal={ENDOCRINOLOGY}, author={Strahl, BD and Huang, HJ and Pedersen, NR and Wu, JC and Ghosh, BR and Miller, WL}, year={1997}, month={Jun}, pages={2621–2631} }