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
Bloodjournal_title
Bloodauthors
Braun A,Gessner JE,Varga-Szabo D,Syed SN,Konrad S,Stegner D,Vögtle T,Schmidt RE,Nieswandt Bdoi
10.1182/blood-2008-05-158477subject
Has Abstractpub_date
2009-01-29 00:00:00pages
1097-104issue
5eissn
0006-4971issn
1528-0020pii
blood-2008-05-158477journal_volume
113pub_type
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