National Academy of Sciences, Proceedings of the National Academy of Sciences, 7(112), p. 2163-2168, 2015
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Significance Interleukin 4 (IL-4) has been shown to be highly protective against delayed type hypersensitivity and organ-specific autoimmune and autoinflammatory reactions in mice and humans, but its mode of action has remained controversial and has failed to be explained solely by redirection of T H 1/T H 17 toward a T H 2-type immune response. Here we uncovered that IL-4 selectively suppresses IL-23 transcription and secretion by cells of the innate immune system. We further describe a previously unidentified therapeutic mode of action of IL-4 in T H 17-mediated inflammation, and a physiologically highly relevant approach to selectively target IL-23/T H 17-dependent inflammation while sparing IL-12 and T H 1 immune responses.