Regulation of lymphocyte function by ORAI and STIM proteins in infection and autoimmunity.

作者: Patrick J. Shaw , Stefan Feske

DOI: 10.1113/JPHYSIOL.2012.233221

关键词: InflammationAutoimmunityEndoplasmic reticulumORAI1STIM1Immune systemCell biologyCalcium signalingLymphocyteBiology

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.

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