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interfering RNA prevented M1 activation, suggesting that SOCS3 is necessary for M1. Wang et al. reported that forced activation of Notch signaling in macrophages enhanced M1 polarization and their anti tumor capacity through SOCS3 induction. Macrophagespecic Aurora B inhibitor SOCS3 cKO mice exhibited resistance to the tumor transplantation model because of reduced tumor promoting cytokines such as TNF and IL 6 and enhanced production of antitumorigenic chemokine MCP2/CCL8. Thus, SOCS3 is an important modulator of macrophage phase and functions. SOCS3 DCs exhibited constitutive activation of STAT3 and expressed low levels of MHC class II molecules, co stimulatory molecules, and IL 12. Adoptive transfer of SOCS3 DCs suppressed

in all hematopoietic cells developed a spectrum of inammatory pathologies with hyper neutrophilia. SOCS3 decient mice developed inammatory neutrophil inltration into multiple tissues and consequent hind leg paresis. SOCS3 has also BI-1356 been shown to inhibit NKT cell activation. In non immune cells, SOCS3 suppresses inammatory reactions by inhibiting STAT3. STAT3 activation is found

HSP differentiation of SOCS3 tg T cells was suppressed. The reciprocal regulation of Th1 and Th17 by SOCS1 and SOCS3 is illustrated in Figure 3. In addition, SOCS1 T cells were less responsive to TGF B, although the mechanism has not yet been claried. Reduced STAT3 activation and TGF B signaling may explain the suppression of Th17 differentiation in SOCS1 decient T cells. Our microarray analysis revealed that T bet, Eomesodermin, and G 1 were upregulated in SOCS1deceint T cells under Th17 skewing conditions, all of which have been reported to suppress Th17 differentiation. Role of SOCS1 and SOCS3 in Th differentiation is summarized in Figures