Abstract
IL-12 is a key regulatory cytokine in cell-mediated immunity and induces the differentiation of naïve T cells towards a TH1 phenotype. The pathogenic activity of IL-12 has been demonstrated in various TH1-mediated experimental models of autoimmune diseases including inflammatory bowel disease (IBD). Moreover, a recent clinical trial showed that targeting of the p40 subunit of IL-12 by neutralizing antibodies suppresses gut inflammation in patients with Crohn's disease. However, since the recently discovered IL-23 shares the p40 subunit with IL-12, the role of IL-12 may have been overestimated in studies using neutralizing p40 antibodies. The discovery that IL-23 but not IL-12 is essential in some models of chronic inflammation and autoimmunity led to a model in which IL-12 is required to induce IFN-gamma producing TH1 cells while IL-23 mediates TH1 effector functions.
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