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 Blood, 15 January 2006, Vol. 107, No. 2, pp. 813-820.
Prepublished online as a Blood First Edition Paper on September 22, 2005; DOI 10.1182/blood-2005-05-1841.

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PHAGOCYTES

The inositol phosphatase SHIP-2 down-regulates Fc{gamma}R-mediated phagocytosis in murine macrophages independently of SHIP-1

Jing Ai, Amita Maturu, Wesley Johnson, Yijie Wang, Clay B. Marsh, and Susheela Tridandapani

From the Molecular, Cellular, and Developmental Biology Program, The Ohio State University; and Department of Internal Medicine, Dorothy M. Davis Heart and Lung Research Institute and Comprehensive Cancer Center, The Ohio State University, Columbus.

Fc{gamma}R-mediated phagocytosis of IgG-coated particles is a complex process involving the activation of multiple signaling enzymes and is regulated by the inositol phosphatases PTEN (phosphatase and tensin homolog deleted on chromosome 10) and SHIP-1 (Src homology [SH2] domain-containing inositol phosphatase). In a recent study we have demonstrated that SHIP-2, an inositol phosphatase with high-level homology to SHIP-1, is involved in Fc{gamma}R signaling. However, it is not known whether SHIP-2 plays a role in modulating phagocytosis. In this study we have analyzed the role of SHIP-2 in Fc{gamma}R-mediated phagocytosis using independent cell models that allow for manipulation of SHIP-2 function without influencing the highly homologous SHIP-1. We present evidence that SHIP-2 translocates to the site of phagocytosis and down-regulates Fc{gamma}R-mediated phagocytosis. Our data indicate that SHIP-2 must contain both the N-terminal SH2 domain and the C-terminal proline-rich domain to mediate its inhibitory effect. The effect of SHIP-2 is independent of SHIP-1, as overexpression of dominant-negative SHIP-2 in SHIP-1-deficient primary macrophages resulted in enhanced phagocytic efficiency. Likewise, specific knockdown of SHIP-2 expression using siRNA resulted in enhanced phagocytosis. Finally, analysis of the molecular mechanism of SHIP-2 down-regulation of phagocytosis revealed that SHIP-2 down-regulates upstream activation of Rac. Thus, we conclude that SHIP-2 is a novel negative regulator of Fc{gamma}R-mediated phagocytosis independent of SHIP-1. (Blood. 2006;107:813-820)


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