Fas-mediated apoptosis in clinical remissions of relapsing experimental autoimmune encephalomyelitis

Journal of Clinical Investigation

Volumn 105, Issue 2, 2000, Pages 223-231

  Suvannavejh, Graig C ^a   Dal Canto, Mauro C ^a   Matis, Louis A ^b   Miller, Stephen D ^a  

^a NORTHWESTERN UNIVERSITY   (United States)

^b ALEXION PHARMACEUTICALS   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

FAS ANTIGEN; GAMMA INTERFERON; LIGAND;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; APOPTOSIS; ARTICLE; AUTOIMMUNE DISEASE; CONTROLLED STUDY; DISEASE COURSE; ENCEPHALOMYELITIS; FEMALE; IMMUNE RESPONSE; MOUSE; NONHUMAN; PRIORITY JOURNAL; RELAPSE; REMISSION; SPINAL CORD; T LYMPHOCYTE;

EID: 0033954469     PISSN: 00219738     EISSN: None     Source Type: Journal    
DOI: 10.1172/JCI8561     Document Type: Article

References (59)

1. Kennedy, M.K., et al. 1990. Inhibition of murine relapsing experimental autoimmune encephalomyelitis by immune tolerance to proteolipid protein and its encephalitogenic peptides. J. Immunol. 144:909-915.
2. McRae, B.L., Kennedy, M.K., Tan, L.J., Dal Canto, M.C., and Miller, S.D. 1992. Induction of active and adoptive chronic-relapsing experimental autoimmune encephalomyelitis (EAE) using an encephalitogenic epitope of proreolipid protein. J. Neuroimmunol. 38:229-240.
3. Brown, A., McFarlin, D.E., and Raine, C.S. 1982. Chronologic neuropathology of relapsing experimental allergic encephalomyelitis in the mouse. Lab. Invest. 46:171-185.
4. Raine, C.S., Mokhtarian, F., and McFarlin, D.E. 1984. Adoptively transferred chronic relapsing experimental autoimmune encephalomyelitis in the mouse. Neuropathologic analysis. Lab. Invest. 51:534-546.
5. McRae, B.L., Vanderlugt, C.L., Dal Canto, M.C., and Miller, S.D. 1995. Functional evidence for epitope spreading in the relapsing pathology of experimental autoimmune encephalomyelitis. J. Exp. Med. 182:75-85.
6. Yu, M., Johnson, J.M., and Tuohy, V.K. 1996. A predictable sequential determinant spreading cascade invariably accompanies progression of experimental autoimmune encephalomyelitis: a basis for peptide-specific therapy after onset of clinical disease. J. Exp Med. 183:1777-1788.
7. Kennedy, M.K., Torrance, D.S., Picha, K.S., Mohler, K.M. 1992. Analysis of cytokine mRNA expression in the central nervous system of mice with experimental autoimmune encephalomyelitis reveals that IL-10 mRNA expression correlates with recovery. J. Immunol. 149:2496-2505.
8. Issazadeh, S., Ljungdahl, A., Hojeberg, B., Mustafa, M., and Olsson, T. 1995. Cytokine production in the central nervous system of Lewis rats with experimental autoimmune encephalomyelitis: dynamics of mRNA expression for IL-10, interleukin-12, cytolysin, tumor necrosis factor alpha, and tumor necrosis beta. J. Neuroimmunol. 61:205-212.
9. Tanuma, N., et al. 1997. Competitive PCR quantification of pro- and anti-inflammatory cytokine mRNA in the central nervous system during autoimmune encephalomyelitis. J. Neuroimmunol. 73:197-206.
10. Racke, M.K., et al. 1991. Prevention and treatment of chronic relapsing experimental allergic encephalomyelitis by transforming growth factor-beta 1. J. Immunol. 146:3012-3017.
11. Rott, O., Fleischer, B., and Cash, E. 1994. Interleukin-10 prevents experimental allergic encephalomyelitis in rats. Eur. J. Immunol. 24:1434-1440.
12. Racke, M.K., et al. 1994. Cytokine-induced immune deviation as a therapy for inflammatory autoimmune disease. J. Exp. Med. 180:1961-1966.
13. Johns, L.D., Flanders, K.C., Ranges, G.E., and Sriram, S. 1991. Successful treatment of experimental allergic encephalomyelitis with transforming growth factor-beta 1. J. Immunol. 147:1792-1796.
14. Racke, M. K., et al. 1992. Evidence of endogenous regulatory function of transforming growth factor-beta 1 in experimental allergic encephalomyelitis. Int. Immunol. 4:615-620.
15. Inobe, J.I., Chen, Y., and Weiner, H.L. 1996. In vivo administration of IL-4 induces TGF-beta-producing cells and protects animals from experimental autoimmune encephalomyelitis. Ann. NY Acad. Sci. 778:390-392.
16. Shaw, M.K., et al 1997 Local delivery of interleukin 4 by retrovirus-transduced T lymphocytes ameliorates experimental autoimmune encephalomyelitis. J. Exp. Med. 185:1711-1714.
17. Begolka, W.S., Vanderlugt, C.L., Rahbe, S.M., and Miller, S.D. 1998. Differential expression of inflammatory cytokines parallels progression of central nervous system pathology in two clinically distinct models of multiple sclerosis. J. Immunol. 161:4437-4446.
18. Begolka, W.S., and Miller, S.D. 1998, Cytokines as intrinsic and exogenous regulators of pachogenesis in experimental autoimmune encephalomyelitis. Res. Immunol. 149:771-781.
19. Bettelli, E., et al. 1998. IL-10 is critical in the regulation of autoimmune encephalomyelitis as demonstrated by studies of IL-10- and IL-4-deficient and transgenic mice. J. Immunol. 161:3299-3306.
20. Wyss-Coray, T., Borrow, P., Brooker, M.J., and Mucke, L. 1997. Astroglial overproduction of TGF-beta 1 enhances inflammatory central nervous system disease in transgenic mice. J. Neuroimmunol. 77:45-50.
21. Cannella, B., Gao, Y.L., Brosnan, C., and Raine, C.S. 1996. IL-10 fails to abrogate experimental autoimmune encephalomyelitis. J. Neurosci. Res. 45:735-746.
22. Sun, D., Qin, Y., Chluba, J., Epplen, J.T., and Wekerle, H. 1988. Suppression of experimentally induced autoimmune encephalomyelitis by cytolytic T-T cell interactions. Nature. 332:843-845.
23. Lider, O., Beraud, E., Reshef, T., Friedman, A., and Cohen, I.R. 1989. Vaccination against experimental autoimmune encephalomyelitis using a subencephalitogenic dose of autoimmune effector T cells. II. Induction of a protective anti-idiotypic response. J. Autoimmun. 2:87-99.
24. Vandenbark, A.A., Hashim, G., and Offner, H. 1989 Immunization with a synthetic T-cell receptor V-region peptide protects against experimental autoimmune encephalomyelitis. Nature 341:541-544.
25. Kumar, V., and Sercarz, E.E. 1993. The involvement of T cell receptor peptide-specific regulatory CD4+ T cells in recovery from antigen-induced autoimmune disease. J. Exp. Med. 178:909-916.
26. Kumar, V., Stellrecht, K., and Sercarz, E. 1996. Inactivation of T cell receptor peptide-specific CD4 regulatory T cells induces chronic experimental autoimmune encephalomyelitis (EAE). J. Exp. Med. 184:1609-1618.
27. + suppressor cells inhibit the function of effector cells of experimental autoimmune encephalomyelitis through a mechanism involving transforming growth factor-beta. J. Immunol. 146:1163-1168
28. Stevens, D.H., Gould, K.E., and Swanborg, R.H. 1994. Transforming growth factor-beta 1 inhibits tumor necrosis factor-alpha/lymphotoxin production and adoptive transfer of disease by effector cells of autoimmune encephalomyelitis. J. Neuroimmunol. 51:77-83.
29. Khoruts, A., Miller, S.D., and Jenkins, M.K. 1995 Neuroantigen-specific Th2 cells are inefficient suppressors of experimental autoimmune encephalomyelitis induced by effector Th1 cells. J. Immunol. 155:5011-5017.
30. Lafaille, J.J., et al. 1997. Myelin basic protein-specific T helper 2 (Th2) cells cause experimental autoimmune encephalomyelitis in immunodeficient hosts rather than protect them from the disease. J. Exp. Med. 186: 307-312.
31. Ware, C. F., VanArsdale, S., and VanArsdale, T.L. 1996. Apoptosis mediated by the TNF-related cytokine and receptor families. J. Cell. Biochem. 60:47-55.
32. Brunner, T., et al. 1995. Cell-autonomous Fas (CD95)/Fas-ligand interaction mediates activation-induced apoptosis in T-cell hybridomas. Nature. 373:441-444.
33. Bonetti, B., Pohl, J., Gao, Y.L., and Raine, C.S. 1997. Cell death during autoimmune demyelination: effector but not target cells are eliminated by apoptosis. J. Immunol. 159:5733-5741.
34. Malipiero, U., et al. 1997. Myelin oligodendrocyte glycoptotein-induced autoimmune encephalomyelitis is chronic/relapsing in perform knock-out mice, but monophasic in Fas- and Fas ligand-deficient lpr and gld mice. Eur. J. Immunol. 27:3151-3160.
35. Becher, B., D'Souza, S.D., Troutt, A.B., and Antel, J.P. 1998. Fas expression on human fetal astrocytes without susceptibility to fas-mediated cytotoxicity. Neuroscience. 84:627-634.
36. Watanabe-Fukunaga, R., Brannan, C.I., Copeland, N.G. Jenkins, N.A., and Nagata, S. 1992. Lymphoproliferation disorder in mice explained by defects in Fas antigen that mediates apoptosis. Nature. 356:314-317.
37. Russell, J.H., Rush, B., Weaver, C., and Wang, R. 1993. Mature T cells of autoimmune lpr/lpr mice have a defect in antigen-stimulated suicide. Proc. Natl. Acad. Sci. USA. 90:4409-4413.
38. Singer, G.G., and Abbas, A.K. 1994. The fas antigen is involved in peripheral but not thymic deletion of T lymphocytes in T cell receptor transgenic mice. Immunity. 1:365-371.
39. Tabi, Z., McCombe, P.A., and Pender, M.P. 1994. Apoptotic elimination of V beta 8.2+ cells from the central nervous system during recovery from experimental autoimmune encephalomyelitis induced by the passive transfer of V beta 8.2+ encephalitogenic T cells. Eur. J. Immunol. 24:2609-2617.
40. White, C.A., McCombe, P.A., and Pender, M.P. 1998. The roles of Fas, Fas Ligand and bcl-2 in T cell apoptosis in the central nervous system in experimental autoimmune encephalomyelitis. J. Neuroimmunol. 82:47-55.
41. Elliott, H.A., et al. 1996. Treatment of experimental encephalomyelitis with a novel chimeric fusion prorein of myelin basic protein and proteolipid protein. J. Clin. Invest. 98:1602-1612.
42. D'Souza, S.D., et al. 1996. Multiple sclerosis: Fas signaling in oligodendrocyte cell death. J. Exp. Med. 184:2361-2370.
43. White, C.A., McCombe, P.A., and Pender, M.P. 1998. Microglia are more susceptible than macrophages to apoptosis in the central nervous system in experimental autoimmune encephalomyelitis through a mechanism not involving Fas (CD95). Int. Immunol. 10:935-941.
44. Tan, L.J., Gordon, K.B., Mueller, J.P., Matis, L.A., and Miller, S.D. 1998. Presentation of proteolipid protein epitopes and B7-1-dependent activation of encephalitogenic T cells by IFN-gamma-activated SJL/J astrocytes. J. Immunol. 160:4271-4279,
45. Cohen, P.L., and Eisenberg, R.A. 1991. Lpr and gld: single gene models of systemic autoimmunity and lymphoproliferative disease. Annu. Rev. Immunol. 9:243-269.
46. Van Parijs, L., Ibraghimov, A., and Abbas, A.K. 1996. The roles of costimulation and Fas in T cell apoptosis and peripheral tolerance. Immunity. 4:521-328.
47. Fuss, I.J., et al. 1997. Characteristic T helper 2 T cell cytokine abnormalities in aucoimmune lymphoproliferative syndrome, a syndrome marked by defective apoptosis and humoral autoimmunity. J. Immunol. 158:1912-1918.
48. Lenardo, M.J. 1991. Interleukin-2 programs mouse αβ T lymphocytes for apoptosis. Nature. 353:858-861.
49. Pender, M.P., McCombe, P.A., Yoong, G., and Nguyen, K.B. 1992. Apoprosis of alpha beta T lymphocytes in the nervous system in experimental autoimmune encephalomyelitis: its possible implications for recovery and acquired tolerance. J. Autoimmun. 5:401-410.
50. Chen, Y., Hancock, W.W., Marks, R., Gonnella, P., and Weiner, H.L. 1999. Mechanisms of recovery from experimental autoimmune encephalomyelitis: T cell deletion and immune deviation in myelin basic protein T cell receptor transgenic mice. J. Neuroimmunol. 82:149-159.
51. Itoh, N., et al. 1997. Requirement of Fas for the development of autoimmune diabetes in nonobese diabetic mice. J. Exp. Med. 186:613-618.
52. Chervonsky, A.V., et al. 1997 The role of Fas in autoimmune diabetes. Cell. 89; 17-24.
53. Suarez-Pinzon, W., et al. 1999. Beta-cell destruction in NOD mice correlates with Fas (CD95) expression on beta-cells and proinflammatory cytokine expression in islets. Diabetes. 48:21-28.
54. Sabelko, K.A., Kelly, K.A., Nahm, M.H., Cross, A.H., and Russell, J.H. 1997. Fas and Fas ligand enhance the pathogenesis of experimental allergic encephalomyelitis, but are not essential for immune privilege in the central nervous system. J. Immunol. 159:3096-3099.
55. Waldner, H., Sobel, R.A., Howard, E., and Kuchroo, V.K. 1997. Fas- and FasL-deficient mice are resistant to induction of autoimmune encephalomyelitis. J. Immunol. 159:3100-3103.
56. Clark, R.B., Grunnet, M., and Lingenheld, E.G. 1997. Adoptively transferred EAE in mice bearing the lpr mutation. Clin. Immunol. Immunopathol. 85:315-319.
57. Sabelko-Downes, K.A., Cross, A.H., and Russell, J.H. 1999. Dual role for Fas ligand in the initiation of and recovery from experimental allergic encephalomyelitis. J. Exp. Med. 189:1195-1205,
58. Dittel, B.N., Merchant, R.M, and Janeway, C.A., Jr. 1999. Evidence for Fas-dependent and Fas-independent mechanisms in the pathogenesis of experimental autoimmune encephalomyelitis. J. Immunol. 162:6392-6400.
59. Vidal, S., Kono, D.H., and Theofilopoulos, A.N. 1998. Loci predisposing to autoimmunity in MRL-Fas lpr and C57B/6-Faslpr mice. J. Clin. Invest. 101:696-702.