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IDDM患者T细胞受体介导的信号通路受损
引用本文:李红梅,仲人前,于嘉屏,曹鲁宁,孔宪涛,陈慰峰. IDDM患者T细胞受体介导的信号通路受损[J]. 细胞与分子免疫学杂志, 2004, 20(2): 222-224
作者姓名:李红梅  仲人前  于嘉屏  曹鲁宁  孔宪涛  陈慰峰
作者单位:1. 上海长征医院临床实验科,上海,200003;北京大学医学部免疫学系,北京,100083
2. 上海长征医院临床实验科,上海,200003
3. 北京大学医学部免疫学系,北京,100083
基金项目:国家自然科学基金资助项目 (No .39730 4 1 0 )
摘    要:目的 :进一步研究IDDM患者T细胞应答改变的机制。方法 :用抗TCR抗体激活患者外周血T细胞 ,分析TCR介导的信号通路的水平。结果 :与正常对照组相比较 ,抗TCR抗体诱导的增殖性应答较弱 (P <0 .0 5) ;rIL 2能部分恢复对抗TCR抗体应答的缺乏 ;抗CD2 8抗体刺激不能恢复TCR介导的增殖性应答 (P =0 .0 3 )。结论 :IDDM患者的T细胞对抗TCR抗体应答的缺乏与TCR介导的信号通路受损有关 ,但协同刺激信号通路正常。TCR信号通路的缺乏增加了IDDM患者T细胞对凋亡的敏感性或无反应性

关 键 词:IDDM  TCR信号通路  缺陷
文章编号:1007-8738(2004)02-0222-03
修稿时间:2003-03-24

Defect of TCR-mediated signal pathway of T cells in IDDM patients
LI Hong-mei ,,ZHONG Ren-qian ,YU Jia-ping ,CAO Lu-ning ,KO NG Xian-tao ,CHEN Wei-feng. Defect of TCR-mediated signal pathway of T cells in IDDM patients[J]. Chinese journal of cellular and molecular immunology, 2004, 20(2): 222-224
Authors:LI Hong-mei     ZHONG Ren-qian   YU Jia-ping   CAO Lu-ning   KO NG Xian-tao   CHEN Wei-feng
Affiliation:Department of Clinical Laboratory, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China.
Abstract:AIM: To study the mechanism responsible for alteration of T cell respons e in IDDM patients. METHODS: T cells from peripheral blood of I DDM patients were activated by anti-TCR antibodies. The level of TCR-mediated signaling pathway was analyzed. RESULTS: T cells from IDDM patients responded weakly to anti- TCR antibody-induced proliferation, as compared with T cells from normal subjec ts (P< 0.05) . The defect could be partially remedied by the addition of rIL-2, while the anti-CD28 antibody stimulation did not restore the prolifera tive response of anti-TCR-induced cells from IDDM patients(P=0.03). CONCLUSION: Underresponsiveness of the T cells from IDDM patients to anti-TCR antibody may result from a defect in the signaling pathway, the CD28 c o-stimulation-signaling pathway is normal. Defect in the TCR signaling pathwa y increases the sensitivity of T cells from IDDM patients to apoptosis or anergy .
Keywords:IDDM  TCR signal pathway  defect
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