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    Immunity. 2011 May 27;34(5):703-14. Epub 2011 Apr 28.

    The calcium sensors STIM1 and STIM2 control B cell regulatory function through interleukin-10 production.

    Matsumoto M, Fujii Y, Baba A, Hikida M, Kurosaki T, Baba Y.

    Source

    Laboratory for Lymphocyte Differentiation, WPI Immunology Frontier Research Center, Osaka University, Suita, Osaka, Japan.

    Abstract

    A chief Ca(2+) entry pathway in immune cells is store-operated Ca(2+) (SOC) influx, which is triggered by depletion of Ca(2+) from the endoplasmic reticulum (ER). However, its physiological role in B cells remains elusive. Here, we show that ER calcium sensors STIM1- and STIM2-induced SOC influx is critical for B cell regulatory function. B cell-specific deletion of STIM1 and STIM2 in mice caused a profound defect in B cell receptor (BCR)-induced SOC influx and proliferation. However, B cell development and antibody responses were unaffected. Remarkably, B cells lacking both STIM proteins failed to produce the anti-inflammatory cytokine IL-10 because of defective activation of nuclear factor of activated T cells (NFAT) after BCR stimulation. This resulted in exacerbation of experimental autoimmune encephalomyelitis, a mouse model of multiple sclerosis. Our data establish STIM-dependent SOC influx as a key signal for B cell regulatory function required to limit autoimmunity.

    Copyright © 2011 Elsevier Inc. All rights reserved.

    PMID:
    21530328
    [PubMed - indexed for MEDLINE]

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