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 Blood, 29 January 2009, Vol. 113, No. 5, pp. 1097-1104.
Prepublished online as a Blood First Edition Paper on October 21, 2008; DOI 10.1182/blood-2008-05-158477.

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PHAGOCYTES, GRANULOCYTES, AND MYELOPOIESIS

STIM1 is essential for Fc{gamma} receptor activation and autoimmune inflammation

Attila Braun1,*, J. Engelbert Gessner2,*, David Varga-Szabo1, Shahzad N. Syed2, Stephanie Konrad2, David Stegner1, Timo Vögtle1, Reinhold E. Schmidt2, and Bernhard Nieswandt1,3

1 Rudolf Virchow Center, Deutsche Forschungsgemeinschaft (DFG) Research Center for Experimental Biomedicine, University of Würzburg, Würzburg; 2 Molecular Immunology Research Unit, Clinic for Immunology and Rheumatology, Hannover Medical School, Hannover; and 3 Institute of Clinical Biochemistry and Pathobiochemistry, University of Würzburg, Würzburg, Germany

Fc{gamma} receptors (Fc{gamma}Rs) 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. FcR{gamma}-based activation is critical in the pathogenesis of these diseases, although the contribution of Fc{gamma}R-mediated calcium signaling in autoimmune injury is unclear. Here we show that macrophages lacking the endoplasmic reticulum–resident calcium sensor, STIM1, cannot activate Fc{gamma}R-induced Ca2+ 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 Fc{gamma}R activation and also indicate that inhibition of STIM1-dependent signaling might become a new strategy to prevent or treat IgG-dependent immunologic diseases.


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