期刊
JOURNAL OF IMMUNOLOGY
卷 174, 期 11, 页码 6582-6586出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.174.11.6582
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CTLA-4-Ig and CD28-Ig are both agonist ligands of B7 coreceptor molecules on mouse dendritic cells (DO), yet they bias the downstream response in opposite directions, and CTLA-4-Ig promotes tolerances whereas CD28-Ig favors the onset of immunity. Although B7 engagement by either ligand leads to a mixed cytokine response, a dominant IL-6 production in response to CD28-Ig prevents the IFN-gamma-driven induction of immunosuppressive trypto-, phan catabolism mediated by IDO. In the present study, we show that silencing the expression of suppressor of cytokine signaling 3 (SOCS3) in DCs by RNA interference renders CD28-Ig capable of activating IDO, likely as a result of unrestrained IFN-gamma signaling and IFN-gamma-like actions of IL-6 Thus, in the absence of SOCS3, CD28-Ig becomes immunosuppressive and mimics the action of CTLA-4-Ig on tryptophan catabolism.
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