摘要
自身免疫性糖尿病是由抗原特异性T淋巴细胞对胰岛β细胞的选择性破坏，凋亡是β细胞破坏的基本过程。凋亡的β细胞所产生的自身抗原通过树突状细胞递呈给幼稚的T淋巴细胞使之活化、进入循环、激发胰岛炎，并通过细胞毒性T细胞再次诱导β细胞凋亡，由此形成恶性循环，导致β细胞强烈而特异性的破坏。环孢菌素A通过对钙调磷酸酶的特异性抑制，下调T淋巴细胞某些早期基因的转录，抑制其活化与增殖，打断β细胞凋亡-T淋巴细胞激活-β细胞凋亡链；环孢菌素A还可能通过阻断钙调磷酸酶介导的线粒体膜通透性转运孔的开放，直接抑制胰岛β细胞凋亡。
The hallmark of autoinmmne diabetes is specific destruction of pancreatic islet beta-cells. The antoantigens coming from the apoptotic beta-cells am taken up and presented to naive autoreaetive T cells by dendritic cells. The activated T lymphoeytes may enter the circulation, and in the islets, they re-encounter co.ate antigen, become reactivated and am retained, thereby initiating insulitis. The eytotoxie T cells can reversely induce the beta-cell apoptosis and ultimately result in the massive and specific destruction of panereatic islet beta-cells. Cyelesporine A （CsA） can inhibit the activation and proliferation of T lymphocyte by down-regulating some early-stage gene expression of T cell, through the specific binding with ealeineurin. CsA may also prevent the beta-cell apoptosis directly by blocking the ealeineurin-mediated opening of the mitoehondrial permeability transition pore （mPIP）. It is the CsA that may break the chain of apoptosis of beta-cells, activation of T lymphoeytes and further apoptosis of beta-cells, while the moleeular signal way and the clinical value on antoinmmne diabetes of CsA is still on study.
出处
《国际内分泌代谢杂志》
2007年第2期101-103,共3页
International Journal of Endocrinology and Metabolism
