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The Journal of Immunology, 2003, 170: 1383-1391.
Copyright © 2003 by The American Association of Immunologists

Suppressor of Cytokine Signaling 1 Inhibits IL-10-Mediated Immune Responses 1

Yaozhong Ding*, Dongmei Chen*, Adel Tarcsafalvi*, Ruthie Su*, Lihui Qin{dagger} and Jonathan S. Bromberg2,*,{ddagger}

* Carl C. Icahn Institute for Gene Therapy and Molecular Medicine, {dagger} Department of Pathology, and {ddagger} Recanati/Miller Transplantation Institute, Mount Sinai School of Medicine, New York, NY 10029

IL-10 has proved to be a key cytokine in regulating inflammatory responses by controlling the production and function of various other cytokines. The suppressor of cytokine signaling (SOCS) gene products are a family of cytoplasmic molecules that are essential mediators for negatively regulating cytokine signaling. It has been previously shown that IL-10 induced SOCS3 expression and that forced constitutive expression of SOCS3 inhibits IL-10/STAT3 activation and LPS-induced macrophage activation. In this report, we show that, in addition to SOCS3 expression, IL-10 induces SOCS1 up-regulation in all cell lines tested, including Ba/F3 pro-B cells, MC/9 mast cells, M1 leukemia cells, U3A human fibroblasts, and primary mouse CD4+ T cells. Induction of SOCS molecules is dependent on STAT3 activation by IL-10R1. Cell lines constitutively overexpressing SOCS proteins demonstrated that SOCS1 and SOCS3, but not SOCS2, are able to partially inhibit IL-10-mediated STAT3 activation and proliferative responses. Pretreatment of M1 cells with IFN-{gamma} resulted in SOCS1 induction and a reduction of IL-10-mediated STAT3 activation and cell growth inhibition. IL-10-induced SOCS is associated with the inhibition of IFN-{gamma} signaling in various cell types, and this inhibition is independent of C-terminal serine residues of the IL-10R, previously shown to be required for other anti-inflammatory responses. Thus, the present results show that both SOCS1 and SOCS3 are induced by IL-10 and may be important inhibitors of both IL-10 and IFN-{gamma} signaling. IL-10-induced SOCS1 may directly inhibit IL-10 IFN-{gamma} signaling, while inhibition of other proinflammatory cytokine responses may use additional IL-10R1-mediated mechanisms.




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