Perkins D L
Renal Division, Laboratory of Immunogenetics and Transplantation, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Curr Opin Nephrol Hypertens. 1998 May;7(3):297-303. doi: 10.1097/00041552-199805000-00010.
Recent progress in experimental models and human genetic linkage studies have provided new insight into the pathogenesis of autoimmunity. Both antigen-specific and antigen-nonspecific signals are crucial in the development of autoimmune disease. Interestingly, several of the single gene loci that have been identified as potential causes of autoimmune disease encode molecules that regulate antigen-nonspecific modulation of immunity. The focus of this review is the role of the opposing signals transduced by the CD28 and cytotoxic T-lymphocyte antigen-4 receptors that bind the B7 costimulatory ligands. Recent studies suggest that CD28 signals activate T cells, whereas cytotoxic T-lymphocyte antigen-4 signals deactivate T cells. importantly, both signals contribute to the induction of autoimmunity and offer novel targets for future therapeutic strategies to treat autoimmune disease.
实验模型和人类基因连锁研究的最新进展为自身免疫性疾病的发病机制提供了新的见解。抗原特异性和抗原非特异性信号在自身免疫性疾病的发展中都至关重要。有趣的是，几个已被确定为自身免疫性疾病潜在病因的单基因位点编码调节免疫抗原非特异性调节的分子。本综述的重点是由结合B7共刺激配体的CD28和细胞毒性T淋巴细胞抗原4受体转导的相反信号的作用。最近的研究表明，CD28信号激活T细胞，而细胞毒性T淋巴细胞抗原4信号使T细胞失活。重要的是，这两种信号都有助于自身免疫的诱导，并为未来治疗自身免疫性疾病的治疗策略提供了新的靶点。
