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National Academy of Sciences, Proceedings of the National Academy of Sciences, 7(112), p. 2163-2168, 2015

DOI: 10.1073/pnas.1416922112

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IL-4 abrogates T <sub>H</sub> 17 cell-mediated inflammation by selective silencing of IL-23 in antigen-presenting cells

Journal article published in 2015 by Emmanuella Guenova, Yuliya Skabytska, Wolfram Hoetzenecker, Günther Weindl ORCID, Karin Sauer, Manuela Tham, Kyu-Won Kim, Ji-Hyeon Park, Ji Hae Seo, Desislava Ignatova, Antonio Cozzio, Mitchell P. Levesque, Thomas Volz, Martin Köberle, Susanne Kaesler and other authors.
This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

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Abstract

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.