关键词: 实验变应性, 受体, 肿瘤坏死因子, 小鼠, 基因敲除, 雪旺氏细胞, 抗原, CD95, 钙磷脂结合蛋白Ⅴ

Abstract: To study the role of Schwann cells apoptosis in the pathogenesis of experimental autoimmune neuritis　(EAN) in TNF receptor Ⅰ knock out　(TNFR Ⅰ－/－)mice. Methods For induction of EAN, TNFRⅠ－/－and wild type C57BL/6 mice were immunized by subcutaneous injection into the back with the peripheral nerve P0 protein peptide 180-199; clinical scores of EAN were assessed and scored immediately before immunization (day 0) and thereafter every other day until day 46 post immunization (p.i.). On day 22 p.i., Schwann cells were collected from　the two groups and cultivated in vitro. The expressions of Fas and Annexin-Ⅴ（Annexin-Ⅴ+/PI－）on Schwann cells from TNFRⅠ－/－ and wild type EAN were detected by flow cytometry. Results More light clinical signs of EAN were observed in the TNFRⅠ－/－ mice（1.50±0.19） than in wild type mice（1.90±0.16）; the percentage of Fas expression on Schwann cells was significantly decreased in TNFRⅠ－/－ mice（88.03%±1.40%)as compared with wild type mice（94.70%±1.53%)(P<0.05). An decreased tendency of Annexin-Ⅴ（Annexin-Ⅴ+/PI－）expression on Schwann cells was seen in TNFRⅠ－/－ mice（8.78%±0.94%)as compared with wild type mice（13.03%±4.15%), but no significant difference. Conclusion TNFRⅠ may induce peripheral nerve injury and aggravate EAN through increasing Schwann cells apoptosis.

Key words: experimental allergic , receptors, tumor necrosis factor, mice, knock out , Swchwann cells, antigens, CD95, Annexin-Ⅴ