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* Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan;
Division of Genome Science, Research Center for Advanced Science and Technology, Tokyo University, Tokyo, Japan; and
Laboratory for Signal Network, Research Center for Allergy and Immunology, RIKEN, Yokohama, Japan
Suppressor of cytokine signaling (SOCS1/JAB) has been shown to play an important role in regulating dendritic cell (DC) function and suppressing inflammatory diseases and systemic autoimmunity. However, role of SOCS1 in DCs for the initiation of Th cell response has not been clarified. Here we demonstrate that SOCS1-deficient DCs induce stronger Th1-type responses both in vitro and in vivo. SOCS1-deficient DCs induced higher IFN-
production from naive T cells than wild-type (WT) DCs in vitro. Lymph node T cells also produced a higher amount of IFN- when SOCS1-deficient bone marrow-derived DCs (BMDCs) were transferred in vivo. Moreover, SOCS1–/– BMDCs raised more effective anti-tumor immunity than WT BMDCs. Microarray analysis revealed that IFN-inducible genes were highly expressed in SOCS1-deficient DCs without IFN stimulation, suggesting hyper STAT1 activation in SOCS1–/– DCs. These phenotypes of SOCS1-deficient DCs were similar to those of CD8
+ DCs, and in the WT spleen, SOCS1 is expressed at higher levels in the Th2-inducing CD4+ DC subset, relative to the Th1-inducing CD8+ DC subset. We propose that reduction of the SOCS1 gene expression in DCs leads to CD8+ DC-like phenotype which promotes Th1-type hyperresponses.
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