Fas has a crucial role in the progression of experimental autoimmune encephalomyelitis

Molecular Immunology

Volumn 35, Issue 5, 1998, Pages 317-326

  Okuda, Yoshinobu ^a   Bernard, Claude C A ^b   Fujimura, Harutoshi ^a   Yanagihara, Takehiko ^a   Sakoda, Saburo ^a  

^a OSAKA UNIVERSITY MEDICAL SCHOOL   (Japan)

^b LA TROBE UNIVERSITY   (Australia)

Author keywords

Cytokine; Experimental autoimmune encephalomyelitis; Fas; Multiple sclerosis; Myelin oligodendrocyte glycoprotein

Indexed keywords

CYTOKINE; FAS ANTIGEN; MESSENGER RNA; MYELIN PROTEIN;

ALLERGIC ENCEPHALOMYELITIS; ANIMAL CELL; ANIMAL MODEL; ANIMAL TISSUE; APOPTOSIS; ARTICLE; CONTROLLED STUDY; DEMYELINATION; FEMALE; GENE EXPRESSION REGULATION; HISTOLOGY; INFLAMMATION; LYMPHOCYTE PROLIFERATION; MOUSE; MULTIPLE SCLEROSIS; NONHUMAN; PRIORITY JOURNAL; REVERSE TRANSCRIPTION POLYMERASE CHAIN REACTION;

ANIMALS; ANTIGENS, CD95; ANTIGENS, SURFACE; APOPTOSIS; CROSSES, GENETIC; CYTOKINES; DEMYELINATING DISEASES; DISEASE PROGRESSION; ENCEPHALOMYELITIS, AUTOIMMUNE, EXPERIMENTAL; EPITOPES; FEMALE; GENE EXPRESSION REGULATION; IMMUNIZATION; IMMUNOGLOBULIN G; LYMPHOCYTE ACTIVATION; MICE; MICE, INBRED C57BL; MICE, INBRED MRL LPR; MYELIN-ASSOCIATED GLYCOPROTEIN; OLIGODENDROGLIA; RNA, MESSENGER; SPINAL CORD; UP-REGULATION;

ANIMALIA;

EID: 0031868315     PISSN: 01615890     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0161-5890(98)00049-2     Document Type: Article

References (36)

1. Adachi, M., Watanabe-Fukunaga, R., Nagata, S., 1993. Aberrant transcription caused by the insertion of an early transposable element in an intron of the Fas antigen gene of lpr mice. Proc. Natl. Acad. Sci. USA 90, 1756-1760.
2. Bernard, C.C.A., Johns, T.G., Slavin, A., Ichikawa, M., Ewing, C., Liu, J., Bettadapura, J., 1997. Myelin oligodendrocyte glycoprotein: a novel candidate autoantigen in multiple sclerosis. J. Mol. Med. 75, 77-88.
3. Bettadapura, J., Menson, K.K., Moritz, S., Liu, J., Bernard, C.C.A., 1998. Expression, purification and encephalitogenicity of recombinant human myelin oligodendrocyte glycoprotein. J. Neurochem., in press.
4. Bonetti, B., Raine, C.S., 1997. Multiple sclerosis: Oligodendrocytes display cell death-related molecules in situ but do not undergo apoptosis. Ann. Neurol. 42, 74-84.
5. Chen, Y., Kuchroo, V.K., Inobe, J., Hafler, D.A., Weiner, H.L., 1994. Regulatory T cell clones induced by oral tolerance: Suppression of autoimmune encephalomyelitis. Science 265, 1237-1240.
6. Chervonsky, A.V., Wang, Y., Wong, F.S., Visintin, I., Flavell, R.A., Janeway Jr., C.A., Matis, L.A., 1997. The role of Fas in autoimmune diabetes. Cell 89, 17-24.
7. Dowling, P., Shang, G., Raval, S., Menonna, J., Cook, S., Husar, W., 1996. Involvement of the CD95 (APO-1/Fas) receptor/ligand system in multiple sclerosis brain. J. Exp. Med. 184, 1513-1518.
8. D'Souza, S.D., Bonetti, B., Balasingam, V., Cashman, N.R., Barker, P.A., Troutt, A.B., Raine, C.S., Antel, J.P., 1996. Multiple sclerosis: Fas signaling in oligodendrocyte cell death. J. Exp. Med. 184, 2361-2370.
9. Ichikawa, H., Ota, K., Iwata, M., 1996. Increased Fas antigen on T cells in multiple sclerosis. J. Neuroimmunol. 71, 125-129.
10. Ichikawa, M., Johns, T.G., Martin, A., Bernard, C.C.A., 1996. Antibody response in Lewis rats injected with myelin oligodendrocyte glycoprotein derived peptides. Int. Immunol. 8, 1667-1674.
11. Ichikawa, M., Johns, T.G., Liu, J., Bernard, C.C.A., 1996. Analysis of the fine B cell specificity during the chronic/relapsing course of a multiple sclerosis-like disease in Lewis rats injected with the encephalitogenic myelin oligodendrocyte glycoprotein peptide 35-55. J. Immunol. 157, 919-926.
12. Inoue, A., Koh, C., Sakai, T., Yamazaki, M., Yanagisawa, N., Usuku, K., Osame, M., 1997. Detection of the soluble form of the Fas molecule in patients with multiple sclerosis and human T-lymphotropic virus type 1-associated myelopathy. J. Neuroimmunol. 75, 141-146.
13. Itoh, N., Imagawa, A., Hanafusa, T., Waguri, M., Yamamoto, K., Iwahashi, H., Moriwaki, M., Nakajima, H., Miyagawa, J., Namba, M., Makino, S., Nagata, S., Kono, N., Matsuzawa, Y., 1997. Requirement of Fas for the development of autoimmune diabetes in nonobese diabetic mice. J. Exp. Med. 186, 613-618.
14. Johns, T.G., Kerlero de Rosbo, N., Menson, K., Abo, S., Gonzales, M.F., Bernard, C.C.A., 1995. Myelin oligodendrocyte glycoprotein induces a demyelinating encephalomyelitis resembling multiple sclerosis. J. Immunol. 154, 5536-5541.
15. 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.
16. Khoury, S.J., Hancock, W.W., Weiner, H.L., 1992. Oral tolerance to myelin basic protein and natural recovery from experimental autoimmune encephalomyelitis are associated with downregulation of inflammatory cytokines and differential upregulation of transforming growth factor β, interleukin 4, and prostaglandin E expression in the brain. J. Exp. Med. 176, 1355-1364.
17. Linington, C., Berger, T., Perry, L., Weerth, S., Hinze-Selch, D., Zhang, Y., Lu, H., Lassmann, H., Wekerle, H., 1993. T cells specific for the myelin oligodendrocyte glycoprotein mediate an unusual autoimmune inflammatory response in the central nervous system. Eur. J. Immunol. 23, 1364-1372.
18. b mice: fine specificity and T cell receptor Vβ expression of encephalitogenic T cells. Eur. J. Immunol. 25, 1951-1959.
19. Nagata, S., 1994. Fas and Fas ligand: a death factor and its receptor. Adv. Immunol. 57, 129-144.
20. Nguyen, K.B., McCombe, P.A., Pender, M.P., 1994. Macrophage apoptosis in the central nervous system in experimental autoimmune encephalomyelitis. J. Autoimmun. 7, 145-152.
21. Okuda, Y., Nakatsuji, Y., Fujimura, H., Esumi, H., Ogura, T., Yanagihara, T., Sakoda, S., 1995. Expression of the inducible isoform of nitric oxide synthase in the central nervous system of mice correlates with the severity of actively induced experimental allergic encephalomyelitis. J. Neuroimmunol. 62, 103-112.
22. Okuda, Y., Sakoda, S., Fujimura, H., Yanagihara, T., 1997. Nitric oxide via an inducible isoform of nitric oxide synthase is a possible factor to eliminate inflammatory cells from the central nervous system of mice with experimental allergic encephalomyelitis. J. Neuroimmunol. 73, 107-116.
23. Okuda, Y., Sakoda, S., Bernard, C.C.A., Yanagihara, T., 1998. The development of autoimmune encephalomyelitis provoked by myelin oligodendrocyte glycoprotein is associated with an up-regulation of both proinflammatory and immunoregulatory cytokines in the central nervous system. J. Interferon Cytokine Res., in press.
24. Raine, C.S., 1994. The Dale E. McFarlin Memorial Lecture: the immunology of the multiple sclerosis lesion. Ann. Neurol. 36, 561-572.
25. Renno, T., Krakowski, M., Piccirillo, C., Lin, J., Owens, T., 1995. TNF-α expression by resident microglia and infiltrating leukocytes in the central nervous system of mice with experimental allergic encephalomyelitis. J. Immunol. 154, 944-953.
26. Russell, J.H., Wang, R., 1993. Autoimmune gld mutation uncouples suicide and cytokine/proliferation pathways in activated, mature T cells. Eur. J. Immunol. 23, 2379-2382.
27. Russell, J.H., Rush, B., Weaver, C., 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.
28. Sabelko, K.A., Kelly, K.A., Nahm, M.H., Cross, A.H., 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.
29. Schluesener, H.J., Sobel, R.A., Linington, C., Weiner, H.L., 1987. A monoclonal antibody against a myelin oligodendrocyte glycoprotein induces relapses and demyelination in central nervous system autoimmune disease. J. Immunol. 139, 4016-4021.
30. Schmied, M., Breitschopf, H., Gold, R., Zischler, H., Rothe, G., Wekerle, H., Lassmann, H., 1993. Apoptosis of T lymphocytes in experimental autoimmune encephalomyelitis. Am. J. Pathol. 143, 446-452.
31. + encephalitogenic T cells. Eur. J. Immunol. 24, 2609-2617.
32. Tabi, Z., McCombe, P.A., Pender, M.P., 1995. Antigen-specific down-regulation of myelin basic protein-reactive T cells during spontaneous recovery from experimental autoimmune encephalomyelitis: further evidence of apoptotic deletion of autoreactive T cells in the central nervous system. Int. Immunol. 7, 967-973.
33. Takahashi, T., Tanaka, M., Brannan, C.I., Jenkins, N.A., Copeland, N.G., Suda, T., Nagata, S., 1994. Generalized lymphoproliferative disease in mice, caused by a point mutation in the Fas ligand. Cell 76, 969-976.
34. Tsukada, I., Fujinami, R.S., 1996. Two models for multiple sclerosis: experimental allergic encephalomyelitis and Theiler's murine encephalomyelitis virus. J. Neuropathol. Exp. Neurol. 55, 673-686.
35. Waldner, H., Sobel, R.A., Howard, E., Kuchroo, V.K., 1997. Fasand FasL-deficient mice are resistant to induction of autoimmune encephalomyelitis. J. Immunol. 159, 3100-3103.
36. Yonehara, S., Ishii, A., Yonehara, M., 1989. A cell-killing monoclonal antibody (anti-Fas) to a cell surface antigen co-downregulated with the receptor of tumor necrosis factor. J. Exp. Med. 169, 1747-1756.