期刊
JOURNAL OF PHYSIOLOGY-LONDON
卷 590, 期 17, 页码 4157-4167出版社
WILEY
DOI: 10.1113/jphysiol.2012.233221
关键词
-
资金
- NIH [AI066128]
- National Multiple Sclerosis Society
Store-operated Ca2+ entry (SOCE) in cells of the immune system is mediated by Ca2+ release-activated Ca2+ (CRAC) channels that are formed by ORAI1 and its homologues ORAI2 and ORAI3. They are activated by stromal interaction molecules (STIM) 1 and 2 in response to depletion of endoplasmic reticulum Ca2+ stores. Loss-of-function mutations in the human ORAI1 and STIM1 genes abolish CRAC channel function and SOCE in a variety of non-excitable cells including lymphocytes and other immune cells, resulting in a unique clinical syndrome termed CRAC channelopathy. It is dominated by severe immunodeficiency and autoimmunity due to impaired SOCE and defects in the function of several lymphocyte subsets. These include CD8+ T cells, CD4+ effector and regulatory T cells, natural killer (NK) cells and B cells. This review provides a concise discussion of the role of CRAC channels in these lymphocyte populations and the regulation of adaptive immune responses to infection, in autoimmunity and inflammation.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据