@article{vahlenkamp_bull_dow_collisson_winslow_phadke_tompkins_tompkins_2004, title={B7(+)CTLA4(+) T cells engage in T-T cell interactions that mediate apoptosis: a model for lentivirus-induced T cell depletion}, volume={98}, ISSN={["0165-2427"]}, DOI={10.1016/j.vetimm.2003.12.006}, abstractNote={Apoptosis in lymph node (LN) T cells of feline immunodeficiency virus (FIV)-infected cats is associated with cells co-expressing B7.1 and B7.2 costimulatory molecules, and their ligand CTLA4. To study the possibility of B7.1/B7.2-CTLA4 mediated T-T interactions and the predicted induction of T cell apoptosis in vitro, costimulatory molecules were up-regulated on CD4+ and CD8+ T cells by mitogen stimulation. B7.1 expression on in vitro stimulated CD4+ and CD8+ cells increased within 24h; B7.2 and CTLA4 expression increased after 48-72 h. Apoptosis, as analyzed by terminal deoxynucleotidyl transferase (transferase nick end labeling, TUNEL)-based staining followed by three color flow cytometric analysis, correlated to the cells expressing B7 and/or CTLA4. Blocking experiments revealed that CD4+ and CD8+ T cell apoptosis could be significantly inhibited with anti-B7 antibodies. As FIV infection results in immune activation with a T cell phenotype similar to that of the in vitro activated T cells, the data support the hypothesis that the chronic expansion of B7+CTLA4+ LN T cells in infected cats allows for T-T cell interactions resulting in T cell depletion and eventually the development of AIDS.}, number={3-4}, journal={VETERINARY IMMUNOLOGY AND IMMUNOPATHOLOGY}, author={Vahlenkamp, TW and Bull, ME and Dow, JL and Collisson, EW and Winslow, BJ and Phadke, AP and Tompkins, WAF and Tompkins, MB}, year={2004}, month={Apr}, pages={203–214} }
 @article{ghatnekar_barnes_dow_smoak_2004, title={Hypoglycemia-induced changes in cell death and cell proliferation in the organogenesis-stage embryonic mouse heart (Retracted article. See vol 76, pg 278, 2006)}, volume={70}, ISSN={["1542-0760"]}, DOI={10.1002/bdra.20000}, abstractNote={Abstract}, number={3}, journal={BIRTH DEFECTS RESEARCH PART A-CLINICAL AND MOLECULAR TERATOLOGY}, author={Ghatnekar, GS and Barnes, JA and Dow, JL and Smoak, IW}, year={2004}, month={Mar}, pages={121–131} }
 @article{bull_vahlenkamp_dow_collisson_winslow_phadke_tompkins_tompkins_2004, title={Spontaneous T cell apoptosis in feline immunodeficiency virus (FIV)-infected cats is inhibited by IL2 and anti-B7.1 antibodies}, volume={99}, ISSN={["1873-2534"]}, DOI={10.1016/j.vetimm.2004.01.010}, abstractNote={Lymph node (LN) T cells from feline immunodeficiency virus (FIV)-infected cats have an increased expression of B7 co-stimulatory molecules as well as their ligand CTLA4, resembling an activation phenotype shown to induce anergy and apoptosis in activated T cells. In addition, LN T cells from FIV-infected cats also show increased spontaneous apoptosis compared to uninfected animals. The apoptosis observed in these animals occurs primarily in T cells expressing B7 and CTLA4, suggesting a role for B7 and CTLA4 interactions in the induction of anergy/apoptosis. In order to investigate the role of B7 and CTLA4 interactions on T cell apoptosis in LN T cells from FIV-infected cats, we performed blocking experiments by measuring T cell apoptosis in LN T cell cultures treated with anti-feline B7.1, B7.2, and CTLA4 specific antibodies, as well as interleukin (IL)-2. The addition of IL2, the primary cytokine produced by B7/CD28 interactions, resulted in a significant decrease of T cell apoptosis in cultured LN cells as assessed by two-color flow cytometry and TUNEL assay. The addition of anti-B7.1 antibodies significantly inhibited T cell apoptosis in FIV-infected cats with low-level plasma viremia, while addition of anti-B7.2 and anti-CTLA4 antibodies had no affect. These results suggest a role of B7 signaling in the increased spontaneous apoptosis observed in LN T cells from FIV-infected animals.}, number={1-2}, journal={VETERINARY IMMUNOLOGY AND IMMUNOPATHOLOGY}, author={Bull, ME and Vahlenkamp, TW and Dow, JL and Collisson, EW and Winslow, BJ and Phadke, AP and Tompkins, MB and Tompkins, WAF}, year={2004}, month={May}, pages={25–37} }
 @article{tompkins_bull_dow_ball_collisson_winslow_phadke_vahlenkamp_tompkins_2002, title={Feline immunodeficiency virus infection is characterized by B7(+)CTLA4(+) T cell apoptosis}, volume={185}, ISSN={["0022-1899"]}, DOI={10.1086/339847}, abstractNote={The B7.1 and B7.2 costimulatory molecules on antigen-presenting cells provide second signals for regulating T cell immune responses via CD28 and cytotoxic T lymphocyte antigen 4 (CTLA4) on T cells. CD28 signals cell proliferation, whereas CTLA4 signals for anergy or apoptosis, terminating the immune response. Because T cell apoptosis and immunodeficiency is a characteristic of feline immunodeficiency virus (FIV)-infected cats, it is possible that negative T cell signaling via B7 and CTLA4 may be favored in these cats. Flow cytometry revealed high percentages of CD8+ and CD4+ cells expressing B7.1, B7.2, and CTLA4 in lymph nodes of FIV-positive cats and a large fraction of CTLA4+ T cells coexpressing B7.1 and B7.2. Three-color analysis with anti-B7.1, anti-B7.2, or anti-CTLA4 and TUNEL (terminal deoxynucleotidyl transferase nick-end-labeling) analysis revealed that apoptosis was a characteristic of B7.1+ B7.2+ CTLA4+ T cells. These data support the hypothesis that lymph node apoptosis and immune deterioration in FIV-infected cats results from chronic B7.1- and/or B7.2-CTLA4-mediated T-T interactions.}, number={8}, journal={JOURNAL OF INFECTIOUS DISEASES}, author={Tompkins, MB and Bull, ME and Dow, JL and Ball, JM and Collisson, EW and Winslow, BJ and Phadke, AP and Vahlenkamp, TW and Tompkins, WA}, year={2002}, month={Apr}, pages={1077–1093} }
 @inproceedings{vahlenkamp_bull_dow_anderson_tompkins_tompkins_2001, title={B7.1/B7.2 and CTLA4 expression on feline T cells in vitro correlates with apoptosis}, number={2001}, booktitle={Journal of Leukocyte Biology}, author={Vahlenkamp, T. W. and Bull, M. E. and Dow, J. and Anderson, J. and Tompkins, M. B. and Tompkins, W. A. F.}, year={2001}, pages={255} }
 @inproceedings{tompkins_bull_dow_tompkins_2001, title={Feline immunodeficiency virus (FIV) infection induces B7(+)CTLA4(+) T cell apoptosis: A model for T cell depletion and immunodeficiency}, number={2001}, booktitle={Journal of Leukocyte Biology}, author={Tompkins, M. B. and Bull, M. E. and Dow, J. L. and Tompkins, W. A. F.}, year={2001}, pages={254} }
 @article{gebhard_dow_childers_alvelo_tompkins_tompkins_1999, title={Progressive expansion of an L-selectin-negative CD8 cell with anti-feline immunodeficiency virus (FIV) suppressor function in the circulation of FIV-infected cats}, volume={180}, ISSN={["0022-1899"]}, DOI={10.1086/315089}, abstractNote={The acute stage of feline immunodeficiency virus (FIV) infection is characterized by the appearance of a major CD8 subpopulation with reduced expression of the CD8 beta chain (CD8alpha+betalo). CD8 antiviral activity was subsequently shown to be mediated by the CD8alpha+betalo phenotype, which is the dominant CD8 phenotype in long-term infected cats. Two- and three-color flow cytometric analysis demonstrated that the CD8alpha+betalo subset is L-selectin negative (CD62L-) and has increased expression of CD44, CD49d, and CD18, consistent with an activation phenotype. The CD8alpha+betaloCD62L- cells but not the CD8alpha+betahiCD62L+ cells demonstrated strong antiviral activity in the FIV acute-infection assay. The progressive expansion of the CD8alpha+betaloCD62L- effector subset cells in FIV-infected cats parallels that seen in human immunodeficiency virus (HIV)-infected patients, suggesting that failure in homeostatic mechanisms regulating lymphocyte activation or trafficking (or both) may be a consequence of both HIV and FIV infections.}, number={5}, journal={JOURNAL OF INFECTIOUS DISEASES}, author={Gebhard, DH and Dow, JL and Childers, TA and Alvelo, JI and Tompkins, MB and Tompkins, WAF}, year={1999}, month={Nov}, pages={1503–1513} }
 @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} }