@article{zhang_reckling_dean_2015, title={Phenotypic and functional analysis of CD1a+dendritic cells from cats chronically infected with feline immunodeficiency virus}, volume={42}, journal={Comparative Immunology, Microbiology and Infectious Diseases}, author={Zhang, L. and Reckling, S. and Dean, G. A.}, year={2015}, pages={53–59} }
 @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{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} }