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• W2149264611 abstract "Abstract IL‐23 is regarded as a major pro‐inflammatory mediator in autoimmune disease, a role which until recently was ascribed to its related cytokine IL‐12. IL‐23, an IL‐12p40/p19 heterodimeric protein, binds to IL‐12Rβ1/IL‐23R receptor complexes. Mice deficient for p19, p40 or IL‐12Rβ1 are resistant to experimental autoimmune encephalomyelitis or collagen‐induced arthritis. Paradoxically, however, IL‐12Rβ2‐ and IL‐12p35‐deficient mice show remarkable increases in disease susceptibility, suggesting divergent roles of IL‐23 and IL‐12 in modulating inflammatory processes. IL‐23 induces IL‐17, which mediates inflammation and tissue remodeling, but the role of IL‐12 in this respect remains unidentified. We investigated the roles of exogenous (recombinant) and endogenous (macrophage‐derived) IL‐12 and IL‐23, on IL‐17‐induction in human T‐cells. IL‐23 enhanced IL‐17 secretion, as did IL‐2, IL‐15, IL‐18 and IL‐21. In contrast, IL‐12 mediated specific inhibition of IL‐17 production. These data support the role of IL‐23 in inflammation through stimulating IL‐17 production by T lymphocytes, and importantly indicate a novel regulatory function for IL‐12 by specifically suppressing IL‐17 secretion. These data therefore extend previous reports that had indicated unique functions for IL‐23 and IL‐12 due to distinct receptor expression and signal transduction complexes, and provide novel insights into the regulation of immunity, inflammation and immunopathology." @default.
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• W2149264611 date "2006-02-28" @default.
• W2149264611 modified "2023-10-15" @default.
• W2149264611 title "Divergent effects of IL-12 and IL-23 on the production of IL-17 by human T cells" @default.
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• W2149264611 doi "https://doi.org/10.1002/eji.200535239" @default.
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