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- W2034160116 endingPage "978" @default.
- W2034160116 startingPage "969" @default.
- W2034160116 abstract "The interleukin (IL)-12 receptor (R)β2 subunit is the critical molecule involved in maintaining IL-12 responsiveness and controlling T helper cell type 1 lineage commitment. We demonstrate that IL-12 and interferon (IFN)-γ play separate, but complementary, roles in regulating IL-12Rβ2 expression on antigen-specific CD4+ T cells. These results are consistent with our previous observation that IL-12 can promote autoimmune disease through IFN-γ–independent as well as –dependent pathways. Therefore, we compared the induction of IL-12 by, and the expression of the IL-12Rβ2 subunit on, myelin basic protein (MBP)-specific T cells from experimental allergic encephalomyelitis (EAE)-susceptible SJL (H-2s) mice and from EAE- resistant B10.S mice (H-2s). B10.S mice had an antigen-specific defect in their capacity to upregulate the IL-12Rβ2 subunit. Defective expression was not secondary to the production of suppressive cytokines, but to a failure of B10.S MBP-specific T cells to upregulate CD40 ligand expression and to induce the production of IL-12. IL-12Rβ2 expression as well as encephalitogenicity of these cells could be restored by the addition of IL-12. These results suggest that the development of immunotherapies that target the IL-12Rβ2 subunit may be useful for the treatment of autoimmune diseases." @default.
- W2034160116 created "2016-06-24" @default.
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- W2034160116 date "1999-03-15" @default.
- W2034160116 modified "2023-10-14" @default.
- W2034160116 title "Regulation of Interleukin (IL)-12 Receptor β2 Subunit Expression by Endogenous IL-12: A Critical Step in the Differentiation of Pathogenic Autoreactive T Cells" @default.
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- W2034160116 doi "https://doi.org/10.1084/jem.189.6.969" @default.
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