Autoimmune lymphoproliferative syndrome: types I, II and beyond.
Autoimmune lymphoproliferative syndrome: types I, II and beyond.
复制标题
自身免疫性淋巴增殖综合征：I 型、II 型及以上。
DOI：
10.1007/978-1-4615-1243-1_6
复制
发表时间：
2001
影响因子：
--
通讯作者：
Lenardo,MJ
中科院分区：
文献类型：
--
作者：
Chun,HJ;Lenardo,MJ
维持免疫系统稳态的一个基本要素是细胞凋亡或程序性细胞死亡的能力。细胞凋亡限制淋巴细胞的积累，并最大限度地减少对自身抗原的反应，可导致自身免疫1，2。淋巴细胞凋亡至少以两种主要形式发生：抗原受体结合和淋巴因子退出。这些形式的死亡是由一种负反馈机制控制的，称为杀本体调节1，3。抗原介导的淋巴细胞死亡受Fas（CD 95/APO-1）、肿瘤坏死因子受体（TNFR）和相关分子4 -6调节。通过淋巴因子退出的被动凋亡可能是由线粒体和Bcl-2蛋白家族成员密切调节的半胱天冬酶的细胞质活化引起的。其他免疫细胞如树突状细胞的凋亡也可能有助于免疫稳态7。
An essential element in the maintenance of homeostasis of the immune system is the capacity for apoptosis, or programmed cell death. Apoptosis limits the accumulation of lymphocytes, and minimizes reactions against self-antigen that can lead to autoimmunity1,2. Lymphocyte apoptosis occurs in at least two major forms: antigen receptor engagement and lymphokine withdrawal. These forms of death are controlled in a negative feedback mechanism termed propriocidal regulation1,3. Antigen-mediated death of lymphocytes is regulated by Fas (CD95/APO-1), tumor necrosis factor receptor (TNFR), and related molecules4-6. Passive apoptosis via lymphokine withdrawal may result from the cytoplasmic activation of caspases that is closely regulated by the mitochondria and the members of the Bcl-2 family of proteins. Apoptosis of other immune cells such as dendritic cells may also contribute to immune homeostasis7.