STIM1 is essential for Fcgamma receptor activation and autoimmune inflammation.

Abstract:

:Fcgamma receptors (FcgammaRs) on mononuclear phagocytes trigger autoantibody and immune complex-induced diseases through coupling the self-reactive immunoglobulin G (IgG) response to innate effector pathways, such as phagocytosis, and the recruitment of inflammatory cells. FcRgamma-based activation is critical in the pathogenesis of these diseases, although the contribution of FcgammaR-mediated calcium signaling in autoimmune injury is unclear. Here we show that macrophages lacking the endoplasmic reticulum-resident calcium sensor, STIM1, cannot activate FcgammaR-induced Ca(2+) entry and phagocytosis. As a direct consequence, STIM1 deficiency results in resistance to experimental immune thrombocytopenia and anaphylaxis, autoimmune hemolytic anemia, and acute pneumonitis. These results establish STIM1 as a novel and essential component of FcgammaR activation and also indicate that inhibition of STIM1-dependent signaling might become a new strategy to prevent or treat IgG-dependent immunologic diseases.

journal_name

Blood

journal_title

Blood

authors

Braun A,Gessner JE,Varga-Szabo D,Syed SN,Konrad S,Stegner D,Vögtle T,Schmidt RE,Nieswandt B

doi

10.1182/blood-2008-05-158477

subject

Has Abstract

pub_date

2009-01-29 00:00:00

pages

1097-104

issue

5

eissn

0006-4971

issn

1528-0020

pii

blood-2008-05-158477

journal_volume

113

pub_type

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