γδ T cells regulate the extent and duration of inflammation in the central nervous system by a fas ligand-dependent mechanism

Journal of Immunology

Volumn 174, Issue 8, 2005, Pages 4678-4687

  Ponomarev, Eugene D ^a   Dittel, Bonnie N ^a  

^a BLOOD RESEARCH INSTITUTE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

CASPASE; FAS LIGAND;

ALLERGIC ENCEPHALOMYELITIS; ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; APOPTOSIS; ARTICLE; BRAIN INJURY; CELL DEATH; CELL FUNCTION; CELL PROLIFERATION; CONTROLLED STUDY; DISEASE DURATION; DISEASE SEVERITY; ENZYME ACTIVITY; INTERMETHOD COMPARISON; MACROPHAGE; MOUSE; NONHUMAN; PRIORITY JOURNAL; T LYMPHOCYTE; WILD TYPE;

EID: 17044374687     PISSN: 00221767     EISSN: None     Source Type: Journal    
DOI: 10.4049/jimmunol.174.8.4678     Document Type: Article

References (35)

1. Born, W., C. Cady, J. Jones-Carson, A. Mukasa, M. Lahn, and R. O'Brien. 1999. Immunoregulatory functions of γδ T cells. Adv. Immunol. 71:77.
2. Mayday, A., and R. Tigelaar. 2003. Immunoregulation in the tissues by γδ T cells. Nat. Rev. Immunol. 3:233.
3. Carding, S. R., and P. J. Egan. 2002. γδ T cells: functional plasticity and heterogeneity. Nat. Rev. Immunol. 2:336.
4. Brunner, T., R. J. Mogil, D. LaFace, N. J. Yoo, A. Mahboubi, F. Echeverri, S. J. Martin, W. R. Force, D. H. Lynch, C. F. Ware, et al. 1995. Cell-autonomous Fas (CD95)/Fas-ligand interaction mediates activation-induced apoptosis in T-cell hybridomas. Nature 373:441.
5. Ju, S. T., D. J. Panka, H. Cui, R. Ettinger, M. El-Khatib, D. H. Sherr, B. Z. Stanger, and A. Marshak-Rothstein. 1995. Fas(CD95)/FasL interactions required for programmed cell death after T-cell activation. Nature 373:444.
6. Huber, S., C. Shi, and R. C. Budd. 2002. γδ T cells promote a Th1 response during coxsackievirus B3 infection in vivo: role of Fas and Fas ligand. J. Virol. 76:6487.
7. Roessner, K., J. Wolfe, C. Shi, L. H. Sigal, S Huber, and R. C. Budd. 2003. High expression of Fas ligand by synovial fluid-derived γδ T cells in Lyme arthritis. J. Immunol. 170:2702.
8. Mukasa, A., M. Lahn, S. Fleming, B. Freiberg, E. Pflum, M. Vollmer, A. Kupfer, R. O'Brien, and W. Born. 2002. Extensive and preferential Fas/Fas ligand-dependent death of γδ T cells following infection with Listeria monocytogenes. Scand. J. Immunol. 56:233.
9. Gao, Y. L., A. J. Rajan, C. S. Raine, and C. F. Brosnan. 2001. γδ cells express activation markers in the central nervous system of mice with chronic-relapsing experimental autoimmune encephalomyelitis. J. Autoimmun. 17:261.
10. Nagata, S., and T. Suda. 1995. Fas and Fas ligand: lpr and gld mutations. Immunol. Today 16:39.
11. Lynch, D. H., F. Ramsdell, and M. R. Alderson. 1995. Fas and FasL in the homeostatic regulation of immune responses. Immunol. Today 16:569.
12. Wong, F. S., B. N. Dittel, and C. A. Janeway, Jr. 1999. Transgenes and knockout mutations in animal models of type 1 diabetes and multiple sclerosis. Immunol. Rev. 169:93.
13. Dittel, B. N., R. M. Merchant, and C. A. Janeway, Jr. 1999. Evidence for Fas-dependent and Fas-independent mechanisms in the pathogenesis of experimental autoimmune encephalomyelitis. J. Immunol. 162:6392.
14. Dittel, B. N. 2000. Evidence that Fas and FasL contribute to the pathogenesis of experimental autoimmune encephalomyelitis. Arch. Immunol. Ther. Exp. 48:381.
15. Sabelko-Downes, K. A., A. H. Cross, and J. H. Russell. 1999. Dual role for Fas ligand in the initiation of and recovery from experimental allergic encephalomyelitis. J. Exp. Med. 189:1195.
16. Okuda, Y., C. C A. Bernard, H. Fujimura, T. Yanagihara, and S. Sakoda. 1998. Fas has a crucial role in the progression of experimental autoimmune encephalomyelitis. Mol. Immunol. 35:317.
17. Suvannavejh, G. C., M. C. Dal Canto, L. A. Matis, and S. D. Miller. 2000. Fas-mediated apoptosis in clinical remissions of relapsing experimental autoimmune encephalomyelitis. J. Clin. Invest. 105:223.
18. Waldner, H., R. A. Sobel, E. Howard, and V. K. Kuchroo. 1997. Fas- and FasL-deficient mice are resistant to induction of autoimmune encephalomyelitis. J. Immunol. 159:3100.
19. Malipiero, U., K. Frei, K. S. Spanaus, C. Agresti, H. Lassmann, M. Hahne, J. Tschopp, H. P. Eugster, and A. Fontana. 1997. Myelin oligodendrocyte glycoprotein-induced autoimmune encephalomyelitis is chronic/relapsing in perform knockout mice, but monophasic in Fas- and Fas ligand-deficient lpr and gld mice. Eur. J. Immunol. 27:3151.
20. Ponomarev, E. D., M. Novikova, M. Yassai, M. Szczepanik, J. Gorski, and B. N. Dittel. 2004. γδ T cell regulation of IFN-γ production by CNS infiltrating encephalitogenic T cells: correlation with recovery from experimental autoimmune encephalomyelitis. J. Immunol. 173:1587.
21. Kobayashi, Y., K. Kawai, K. Ito, H. Honda, G. Sobue, and Y. Yoshikai. 1997. Aggravation of murine experimental allergic encephalomyelitis by administration of T-cell receptor γδ-specific antibody. J. Neuroimmunol. 73:169.
22. Matsumoto, Y., K. Kohyama, Y. Aikawa, T. Shin, Y. Kawazoe, Y. Suzuki, and N. Tanuma. 1998. Role of natural killer cells and TCR γδ T cells in acute autoimmune encephalomyelitis. Eur. J. Immunol. 28:1681.
23. Rajan, A. J., Y. L. Gao, C. S. Raine, and C. F. Brosnan. 1996. A pathogenic role for γδ T cells in relapsing-remitting experimental allergic encephalomyelitis in the SJL mouse. J. Immunol. 157:941.
24. Spahn, T. W., S. Issazadah, A. J. Salvin, and H. L. Weiner. 1999. Decreased severity of myelin oligodendrocyte glycoprotein peptide 33-35-induced experimental autoimmune encephalomyelitis in mice with a disrupted TCR δ chain gene. Eur. J. Immunol. 29:4060.
25. Komoriya, A., B. Z. Packard, M. J. Brown, M. L. Wu, and P. A. Henkart. 2000. Assessment of caspase activities in intact apoptotic thymocytes using cell-permeable fluorogenic caspase substrates. J. Exp. Med. 191:1819.
26. O'Brien, R. L., Y. X. Fu, R. Cranfill, A. Dallas, C. Ellis, C. Reardon, J. Lang, S. R. Carding, R. Kubo, and W. Born. 1992. Heat shock protein Hsp60-reactive γδ cells: a large, diversified T-lymphocyte subset with highly focused specificity. Proc. Natl. Acad. Sci. USA 89:4348.
27. D'Souza, C. D., A. M. Cooper, A. A. Frank, R. J. Mazzaccaro, B. R. Bloom, and I. M. Orme. 1997. An anti-inflammatory role for γδ T lymphocytes in acquired immunity to Mycobacterium tuberculosis. J. Immunol. 158:1217.
28. Kaufmann, S. H., C. Blum, and S. Yamamoto. 1993. Crosstalk between α/β T cells and γ/δ T cells in vivo: activation of α/β T-cell responses after γ/δ T-cell modulation with the monoclonal antibody GL3. Proc. Natl. Acad. Sci. USA 90:9620.
29. Fu, Y. X., C. E. Roark, K. Kelly, D. Drevets, P. Campbell, R. O'Brien, and W. Born. 1994. Immune protection and control of inflammatory tissue necrosis by γδ T cells. J. Immunol. 153:3101.
30. Mombaerts, P., J. Arnoldi, F. Russ, S. Tonegawa, and S. H. E. Kaufmann. 1993. Different roles of αβ and γδ T cells in immunity against an intracellular bacterial pathogen. Nature 365:53.
31. Cardona, A. E., and J. M. Teale. 2002. γ/δ T cell-deficient mice exhibit reduced disease severity and decreased inflammatory response in the brain in murine neurocysticercosis. J. Immunol. 169:3163.
32. Rajan, A. J., V. C. Asensio, I. L. Campbell, and C. F. Brosnan. 2000. Experimental autoimmune encephalomyelitis on the SJL mouse: effect of γδ T cell depletion on chemokine and chemokine receptor expression in the central nervous system. J. Immunol. 164:2120.
33. Godiska, R., D. Chantry, G. N. Dietsch, and P. W. Gray. 1995. Chemokine expression in murine experimental allergic encephalomyelitis. J. Neuroimmunol. 58:167.
34. Sørensen, T. L., M. Tani, J. Jensen, V. Pierce, C. Lucchinetti, V. A. Folcik, S. Qin, J. Rottman, F. Sellebjerg, R. M. Strieter, et al. 1999. Expression of specific chemokines and chemokine receptors in the central nervous system of multiple sclerosis patients. J. Clin. Invest. 103:807.
35. high γδ T cells in Lyme arthritis. J. Exp. Med. 184:2109.