Perforin-independent β-cell destruction by diabetogenic CD8+ T lymphocytes in transgenic nonobese diabetic mice

Journal of Clinical Investigation

Volumn 103, Issue 8, 1999, Pages 1201-1209

  Amrani, Abdelaziz ^a   Verdaguer, Joan ^a   Anderson, Brad ^a   Utsugi, Toshihiro ^b   Bou, Sonny ^a   Santamaria, Pere ^a  

^a UNIVERSITY OF CALGARY   (Canada)

^b GUNMA UNIVERSITY   (Japan)

Author keywords

[No Author keywords available]

Indexed keywords

CD8 ANTIGEN; MAJOR HISTOCOMPATIBILITY ANTIGEN CLASS 1; PERFORIN;

ANIMAL CELL; ANTIGEN PRESENTING CELL; ANTIGENICITY; ARTICLE; AUTOIMMUNE DISEASE; CELL DAMAGE; CELL DIFFERENTIATION; CELL KILLING; CLONAL ANERGY; CYTOTOXIC T LYMPHOCYTE; DIABETOGENESIS; GENE ACTIVATION; INSULIN RESISTANCE; INSULITIS; MOUSE; NONHUMAN; PANCREAS ISLET BETA CELL; PRIORITY JOURNAL; T LYMPHOCYTE ACTIVATION; TARGET CELL;

EID: 0033560930     PISSN: 00219738     EISSN: None     Source Type: Journal    
DOI: 10.1172/JCI6266     Document Type: Article

References (47)

1. Delovitch, T., and Singh, B. 1997. The nonobese diabetic mouse as a model of autoimmune diabetes: immune disregulation gets the NOD. Immunity. 7:727-738.
2. Tisch, R., and McDevitt, H. 1996. Insulin-dependent diabetes mellitus. Cell. 85:291-297.
3. Bendelac, A., Carnaud, C., Boitard, C., and Bach, J.F. 1987. Syngeneic transfer of autoimmune diabetes from diabetic NOD mice to healthy neonates. J. Exp. Med. 166:823-832.
4. Miller, B.J., Appel, M.C., O'Neil, J.J., and Wicker, L.S. 1988. Both the Lyt2+ and L3T4+ T cell subsets are required for the transfer of diabetes in non-obese diabetic mice. J. Immunol. 140:52-58.
5. Yagi, H., et al. 1992. Analysis of the roles of CD4+ and CD8+ T cells in autoimmune diabetes of NOD mice using transfer to NOD athymic nude mice. Eur. J. Immunol. 22:2387-2393.
6. Christianson, S., Shultz, L., and Leiter, E. 1993. Adoptive transfer of diabetes into immunodeficient NOD-scid/scid mice. Relative contributions of CD4+ and CD8+ T cells from diabetic versus prediabetic NOD.NON-thy-1a donors. Diabetes. 42:44-55.
7. Reich, E.P., Sherwin, R.S., Kanagawa, O., andJaneway, C.A., Jr. 1989. An explanation for the protective effect of the MHC class III-E molecule in murine diabetes. Nature. 341:326-328.
8. Haskins, K., and McDuffie, M. 1990. Acceleration of diabetes in young NOD mice with a CD4+ islet-specific T cell clone. Science. 249:1433-1436.
9. Nakano, N., Kikutani, H., Nishimoto, H., and Kishimoto, T. 1991. T cell receptor V gene usage of islet beta cell-reactive T cells is not restricted in non-obese diabetic mice. J. Exp. Med. 173:1091-1097.
10. Bradley, B., Haskins, K., Rosa, F.L., and Lafferty, K. 1992. CD8 T cells are not required for islet destruction induced by a CD4+ islet-specific T-cell clone. Diabetes. 41:1603-1608.
11. Daniel, D., Gill, R., Schloot, N., and Wegmann, D. 1995. Epitope specificity, cytokine production profile and diabetogenic activity of insulin-specific T cell clones isolated from NOD mice. Eur. J. Immunol. 25:1056-1062.
12. Katz, J., Benoist, C., and Mathis, D. 1995. T helper cell subsets in insulin-dependent diabetes. Science. 268:1185-1188.
13. Peterson, J., and Haskins, K. 1996. Transfer of diabetes in the NOD-scid mouse by CD4 T cell clones. Differential requirement for CD8 T cells. Diabetes. 45:328-336.
14. Serreze, D., and Leiter, E. 1994. Genetic and pathogenic basis of autoimmune diabetes in NOD mice. Curr. Opin. Immunol. 6:900-906.
15. Wong, F.S., Visintin, I., Wen, L., Flavell, R., and Janeway, C.A., Jr. 1996. CD8 T cell clones from young NOD islets can transfer rapid onset of diabetes in NOD mice in the absence of CD4 T cells. J. Exp. Med. 183:67-76.
16. Katz, J., Benoist, C., and Mathis, D. 1993. Major histocompatibility complex class I molecules are required for the generation of insulitis in nonobese diabetic mice. Eur. J. Immunol. 23:3358-3360.
17. Wicker, L., et al. 1994. β2-microglobulin-deficient NOD mice do not develop insulitis or diabetes. Diabetes. 43:500-504.
18. null mice are diabetes and insulitis resistant. Diabetes. 43:505-508.
19. Wang, B., Gonzalez, A., Benoist, C., and Mathis, D. 1996. The role of CD8+ T cells in initiation of insulin-dependent diabetes mellitus. Eur. J. Immunol. 26:1762-1769.
20. null nonobese diabetic mice. J. Immunol. 157:3688-3693.
21. Serreze, D., et al. 1997. Initiation of autoimmune diabetes in NOD/Lt mice is MHC class I-dependent. J. Immunol. 157:3978-3986.
22. Kagi, D., et al. 1994. Cytotoxicity mediated by T cells and natural killer cells is greatly impaired in perforin-deficient mice. Nature. 369:31-37.
23. Kagi, D., et al. 1994. Fas and perforin pathways as major mechanisms of T cell-mediated cytotoxicity. Science. 265:528-530.
24. Kojima, H., et al. 1994. Two distinct pathways of specific killing revealed by perforin-mutant cytotoxic T lymphocytes. Immunity. 1:357-364.
25. Hanabuchi, S., et al. 1994. Fas and its ligand in a general mechanism of T-cell mediated cytotoxicity. Proc. Natl. Acad. Sci. USA. 91:4930-4934.
26. Lowin, B., Beermann, F., Schmidt, A., and Tschopp, J. 1994. A null mutation in the perforin gene impairs cytolytic T lymphocyte- and natural killer cell-mediated cytotoxicity. Proc. Natl. Acad. Sci. USA. 91:11571-11575.
27. Walsh, C., et al. 1994. Immune function in mice lacking the perforin gene. Proc. Natl. Acad Sci. USA. 91:10854-10858.
28. Berke, G. 1995. The CTL's kiss of death. Cell. 81:9-12.
29. Kagi, D., Odermatt, B., Ohashi, P., Zinkernagel, R., and Hengartner, H. 1996. Development of insulitis without diabetes in transgenic mice lacking perforin-dependent cytotoxicity. J. Exp. Med. 183:2143-2152.
30. Chervonsky, A., et al. 1997. The role of Fas in autoimmune diabetes. Cell. 89:17-24.
31. Kagi, D., et al. 1997. Reduced incidence and delayed onset of diabetes in perforin-deficient nonobese diabetic mice. J. Exp. Med. 186:989-997.
32. Itoh, N., et al. 1997. Requirement of Fas for the development of autoimmune diabetes in nonobese diabetic mice. J. Exp. Med. 186:613-618.
33. Verdaguer, J., et al. 1997. Spontaneous autoimmune diabetes in monoclonal T cell nonobese diabetic mice. J. Exp. Med. 186:1663-1676.
34. DiLorenzo, T., et al. 1998. MHC class I-restricted T cells are required for all but end stages of diabetes development and utilize a prevalent T cell receptor a chain gene rearrangement. Proc. Natl. Acad. Sci. USA. 95:12538-12542.
35. Wang, F.S., et al. 1998. The role of lymphocyte subsets in accelerated diabetes in nonobese diabetic-rat insulin promoter-B7.1 (NOD-RIP-B7-1) mice. J. Exp. Med. 187:1985-1993.
36. Wallny, H., et al. 1992. Identification and quantitation of a naturally presented peptide as recognized by cytotoxic T lymphocytes specific for an immunogenic tumor variant. Int. Immunol. 4:1085-1090.
37. Verdaguer, J., et al. 1996. Acceleration of spontaneous diabetes in TCRβ-transgenic nonobese diabetic mice by beta cell-cytotoxic CD8+ T cells expressing identical endogenous TCRα chains. J. Immunol. 157:4726-4735.
38. Santamaria, P., et al. 1995. Beta cell cytotoxic CD8+ T cells from nonobese diabetic mice use highly homologous T cell receptor alpha chain CDR3 sequences. J. Immunol. 154:2494-2503.
39. Ohashi, P., et al. 1991. Ablation of tolerance and induction of diabetes by virus infection in viral antigen transgenic mice. Cell. 65:305-317.
40. Wicker, L., Todd, J., and Peterson, L. 1995. Genetic control of autoimmune diabetes in the NOD mouse. Annu. Rev. Immunol. 13:179-200.
41. Hultgren, B., Huang, X., Dybal, N., and Stewart, T. 1996. Genetic absence of γ-interferon delays but does not prevent diabetes in NOD mice. Diabetes. 45:812-817.
42. Herrath, M.V., and Oldstone, M. 1996. Interferon γ is essential for destruction of beta cells and development of insulin-dependent diabetes mellitus. J. Exp. Med. 185:531-539.
43. Cao, W., Tykodi, S., Esser, M., Braciale, V., and Braciale, T. 1995. Partial activation of CD8+ T cells by a self-derived peptide. Nature. 378:295-298.
44. Muller, C., et al. 1989. Detection of perforin and granzyme A mRNAs in infiltrating cells during LCMV infection of mice. Eur. J. Immunol. 19:1253-1259.
45. Leithäuser, F., et al. 1993. Constitutive and induced expression of APO-1, a new member of the nerve growth factor/tumor necrosis factor receptor superfamily, in normal and neoplastic cells. Lab. Invest. 69:415-429.
46. Stassi, G., et al. 1995. Expression of apoptosis-inducing CD95 (Fas/Apo-1) on human beta cells sorted by flow cytometry and cultured in vitro. Transplant. Proc. 27:3271-3275.
47. Yamada, K., Takane-Gyotoku, N., Ichikawa, F., Inada, C., and Nokada, K. 1996. Mouse islet cell lysis mediated by interleukin-1-induced Fas. Diabetologia. 39:1306-1312.