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

2015; National Academy of Sciences; Volume: 112; Issue: 7 Linguagem: Inglês

10.1073/pnas.1416922112

1091-6490

Emmanuella Guenova, Yuliya Skabytska, Wolfram Hoetzenecker, Günther Weindl, 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, Peter Thomas, Reinhard Mailhammer, Kamran Ghoreschi, Knut Schäkel, Boyko Amarov, Martin Eichner, Martin Schaller, Rachael A. Clark, Martin Röcken, Tilo Biedermann,

Dermatology and Skin Diseases

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.