作者: Patrick J. Shaw , Stefan Feske
DOI: 10.1113/JPHYSIOL.2012.233221
关键词: Inflammation 、 Autoimmunity 、 Endoplasmic reticulum 、 ORAI1 、 STIM1 、 Immune system 、 Cell biology 、 Calcium signaling 、 Lymphocyte 、 Biology
摘要: Store-operated Ca(2+) entry (SOCE) in cells of the immune system is mediated by release-activated (CRAC) channels that are formed ORAI1 and its homologues ORAI2 ORAI3. They activated stromal interaction molecules (STIM) 1 2 response to depletion endoplasmic reticulum stores. Loss-of-function mutations human STIM1 genes abolish CRAC channel function SOCE a variety non-excitable including lymphocytes other cells, resulting unique clinical syndrome termed channelopathy. It dominated severe immunodeficiency autoimmunity due impaired defects several lymphocyte subsets. These include CD8(+) T CD4(+) effector regulatory natural killer (NK) B cells. This review provides concise discussion role these populations regulation adaptive responses infection, inflammation.