期刊文献+

EAE大鼠中枢神经系统与外周免疫器官细胞凋亡的研究 被引量:6

A Study of Cell Apoptosis in the Central Nervous System and the Peripheral Lymphoid Organs in EAE Rats
下载PDF
导出
摘要 目的 比较实验性自身免疫性脑脊髓炎 ( experimental autoimmune encephalomyelitis,EAE)大鼠中枢神经系统 ( CNS)与外周免疫器官中细胞的凋亡情况。方法 建立 EAE大鼠模型 ,于病程不同阶段取脊髓与外周免疫器官通过脱氧核糖核苷酸末端转移酶介导的缺口末端标记 ( TUNEL)技术检测细胞凋亡情况。结果 脊髓中细胞凋亡现象具有明显的时程特异性 ,凋亡细胞主要为淋巴细胞、巨噬细胞和小胶质细胞 ;脾和淋巴结中TUNEL阳性细胞数目均较少 ,且组内与组间差异均无显著性。结论  EAE外周免疫器官与 Objective To study the apoptotic lymphoid cells in the central nervous system (CNS) and the peripheral lymphoid organs in experimental autoimmune encephalomyelitis (EAE) rats. Methods Lymph nodes, spleens and lumbar spinal cords were removed form EAE rats at various stages of the course, and embeded with paraffin for cytochemical TUNEL detection. Results The number of TUNEL positive cells has an obvious course related character in the spinal cord in EAE, and the majority of TUNEL positive cells were T cells,macrophages and microglia judged by the morphological features. TUNEL positive cells could be found occasionally in the lymph nodes and spleens, while no significant difference was found between the two groups. Conclusions The various environmental conditions in CNS and peripheral lymphoid organs may affect the occurrence of apoptosis.
出处 《中国神经免疫学和神经病学杂志》 CAS 2004年第5期280-282,共3页 Chinese Journal of Neuroimmunology and Neurology
基金 河北省卫生厅基金资助项目 (2 0 0 1-0 10 5 4)
关键词 实验性自身免疫性脑脊髓炎 外周免疫器官 细胞凋亡 experimental autoimmune encephalomyelitis peripheral lymphoid organs apoptosis
  • 相关文献

参考文献11

  • 1[1]Petry KG,Boullerne AI, Pousset F, et al. Experimental allergic encephalomyelitis animal models for analyzing features of multiple sclerosis [J]. Pathol Biol (Paris), 2000,48(1):47-53.
  • 2[2]Tabi Z, McCombe PA, Pender MP. 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[J]. Int Immunol, 1995, 7(6):967-973.
  • 3[3]Pender MP. Activation-induced apoptosis of autoreactive and alloreactive T lymphocytes in the target organ as a major mechanism of tolerance [J]. Immunol Cell Biol, 1999,77(3): 216-223.
  • 4[4]Suvannavejh GC, Dal Canto MC, Matis LA, et al.Fas-mediated apoptosis in clinical remissions of relapsing experimental autoimmune encephalomyelitis [J]. J Clin Invest, 2000,105(2):223-231.
  • 5[5]Pender MP,Rist MJ. Apoptosis of inflammatory cells in immune control of the nervous system: role of glia [J]. Glia, 2001,36(2) :137-144.
  • 6[6]White CA, McCombe PA, Pender MP. The roles of Fas, Fas ligand and Bcl-2 in T cell apoptosis in the central nervous system in experimental autoimmune encephalomyelitis [J]. J Neuroimmunol, 1998, 82(1):47-55.
  • 7[7]Ishigami T, White CA, Pender MP. Soluble antigen therapy induces apoptosis of autoreactive T cells pre ferentially in the target organ rather than in the peripheral lymphoid organs [J]. Eur J Immunol,1998,28(5): 1626-1635.
  • 8[8]Shapira L, Ayalon S,Brenner T. Effects of porphyromonas gingivalis on the central nervous system:activation of glial cells and exacerbation of experimental autoimmune encephalomyelitis [J]. J Periodontol, 2002,73 (5): 511-516.
  • 9王惠,林嘉友,杨天祝.实验性变态反应性脑脊髓炎与细胞凋亡[J].中国神经免疫学和神经病学杂志,2000,7(3):175-179. 被引量:4
  • 10[10]Engelhardt B. Role of glucocorticoids on T cell recruitment across the blood-brain barrier [J]. Z Rheumatol, 2000,59(suppl 2): Ⅱ/18-21.

二级参考文献18

  • 1[1] Zielasek J, Jung S, Gold R, et al. Adm inistration of nitric oxide synth ase inhibitors in experimental autoimmune neuritis and experimental autoimmun e encephalomyelitis[J]. J Neuroimmunol, 1995,58:81-88.
  • 2[2] Cross AH, Misko TP, Lin RF, et al. Aminoguanidi ne, an inhibitor of indu cible nitric oxide synthase, ameliorates experimental autoimmune encephalomyelit is in SJL mice[J]. J Clin Invest, 1994,93:2684-2690.
  • 3[3] Sabelko KA, Kelly KA, Nahm MH, et al. Fas and Fas ligand enhance the pathogensis of experimental allergic encephalomyelitis, but are not essential fo r immune privilege in the central nervous system[J]. J Immunol, 1997,159 :3096-3099.
  • 4[4] Waldner H, Sobel RA, Howard E, et al. Fas- and Fas-L-deficient mice are resistant to induction of autoimmune encephalomyelitis[J]. J Immunol, 1997,159:3100-3103.
  • 5[5] Okuda Y, Bernard CCA, Fujimura H, et al. Fas ha s a crucial role in the progression of experimental autoimmune encephalomyelitis[J]. Mol Immunol, 1998 ,35(5):317-326.
  • 6[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[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[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[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[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.

共引文献3

同被引文献58

引证文献6

二级引证文献10

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部