[6] D`Souza SD, Bonetti B, Balasingam V, et al. Mul tiple slcerosis: Fas si gnaling in oligodendrocyte cell death[J]. J Exp Med, 1996,184:2361-237 0.
[7] Nguyen KB, McCombe PA,Pender MP. Macrophage apopt osis in the central n ervous system in experimental autoimmune encephalomyelitis[J]. J Autoimmun, 1994,7:145-152.
[8] Bonetti B, Pohl J, Gao YL, et al. Cell death du ring autoimmune demyeli nation:effector but not target cells are eliminated by apoptosis[J]. J Immun ol, 1997,159:5733-5741.
[9] Tabi Z, McCombe PA,Pender MP. Apoptic elimination of Vβ 8.2+ cells f rom the central nervous system during recovery from experimental autoimmune enc ephalitogenic T cells[J]. Eut J Immunol, 1994,24:2609-2617.
[10] McCombe PA, Nickson I, Tabi Z, et al. Apoptosis of V beta 8.2+ T ly mphocytes in the spinal cord during recovery from experimental autoimmune encep halomyelitis induced in Lewis rats by inoculation with myelin basic protein K[ J]. Neurol Sci, 1996,139(1):1-6.
[11] Tabi Z, McCombe PA,Pender MP. Antigen-specific d own-regulation of my elin basic protein-reactive T cells during spontaneous recovery from experimen t al autoimmune encephalomyelitis: futher evidence of apoptic deletion of autorea ctive T cells in the central nervous system[J]. Inter Immunol, 1995,7(6) :967-973.
[12] White CA, McCombe PA, Pender MP. The roles of Fas , Fas ligand and Bcl-2 i n T cell apoptosis in the central nervous system in experimental autoimmune enc ephalomyelitis[J]. J Neuroimmunol, 1998,82:47-55.
[13] Chen Y, Hancock WW, Marks R, et al. Mechanism of recovery from expe rimental autoimmune encephalomyelitis: T cell deletion and immune deviation in myelin basic protein T cell receptor transgenic mice[J]. J Neuroimmul, 1998,82:149-159.
[14] Kohji T, Tanuma N, Aikaua Y, et al. Interactio n between apoptic cells and reactive brain cells in the central nervous system of rats with autoimmune encephalomyelitis[J]. J Neuroimmunol, 1998,82:168-174.
[15] White CA, McCombe PA, Pender MP. Microglia are mor e susceptible than macr ophages to apoptosis in the central nervous system in experimental autoimmune e ncephalomyelitis through a mechanism not involving Fas (CD95)[J]. Int Immunol , 1998,10(7):935-941.
[16] Smith T, Schmied M, Hewson AK, et al. Apoptosi s of T cells and macrop hages in the central nervous system of intact and adrenalectimized Lewis rats d uring experimental allergic encephalomyelitis[J]. J Autoimmun, 1996,9(2 ):167-174.
[17] Okuda Y, Sakoda S, Fujimura H, et al. Nitric o xide via an inducible i soform of nitric oxide synthase is a possible factor to eliminate inflammatory cells from the central nervous system of mice with experimental allergic enceph alomyelitis[J]. J neuroimmunol, 1997,73(1-2):107-116.
[18] Zettl UK, Mix E, Zielasek J, et al. Apoptosis of myelin-reac tive T cells induced by reactive-oxygen and nitrogen intermediates in vitro [J]. Cell immunol, 1997,178:1-8.