PD-1/PD-L pathway and autoimmunity
PD-1/PD-L pathway and autoimmunity
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DOI：
10.1080/08916930500124072
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发表时间：
2005-08-01
期刊：
影响因子：
3.5
通讯作者：
Wang, P
中科院分区：
文献类型：
--
作者：
Okazaki, T;Wang, P
程序性细胞死亡1 （PD-1）是在1992年通过减法杂交技术分离出来的，它是一个在凋亡刺激下表达增强的分子。从那时起，我们一直在分析PD-1在调节免疫反应中的功能。PD-1缺陷小鼠的产生、PD-1缺陷小鼠自身免疫性疾病的病理生理分析、两种配体的鉴定以及PD-1下游事件的分析表明，PD-1通过抑制自身反应性淋巴细胞的激活来阻止自身免疫。这些发现被进一步应用于人类自身免疫性疾病，人类PD- 1基因的单核苷酸多态性（snp）已被报道与系统性红斑狼疮（SLE）、类风湿性关节炎（RA）和I型糖尿病有关。
Programmed cell death 1 (PD-1) was isolated in 1992 by subtractive-hybridization technique, as a molecule whose expression is enhanced by apoptotic stimuli. Since then we have been analyzing the function of PD-1 in the regulation of immune responses. Generation of PD-1 deficient mice, pathophysiological analyses of autoimmune diseases in PD-1 deficient mice, identification of two ligands, and analyses of downstream events of PD-1 revealed that PD-1 prevents autoimmunity by inhibiting activation of self-reactive lymphocytes. These findings were further applied on human autoimmune diseases and single nucleotide polymorphisms (SNPs) on human PD- I gene have been reported to link with systemic lupus erythematosus (SLE), rheumatoid arthritis (RA) and type I diabetes.