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IL-38 Ameliorates Skin Inflammation and Limits IL-17 Production from γδ T Cells

 
: Han, Y.; Mora, J.; Huard, A.; Silva, P. da; Wiechmann, S.; Putyrski, M.; Schuster, C.; Elwakeel, E.; Lang, G.; Scholz, A.; Scholz, T.; Schmid, T.; Bruin, N. de; Billuart, P.; Sala, C.; Burkhardt, H.; Parnham, M.J.; Ernst, A.; Brüne, B.; Weigert, A.

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Volltext ()

Cell reports 27 (2019), Nr.3, S.835-846.e5
ISSN: 2211-1247
Englisch
Zeitschriftenaufsatz, Elektronische Publikation
Fraunhofer IME ()

Abstract
Interleukin-38 (IL-38) is a cytokine of the IL-1 family with a role in chronic inflammation. However, its main cellular targets and receptors remain obscure. IL-38 is highly expressed in the skin and downregulated in psoriasis patients. We report an investigation in cellular targets of IL-38 during the progression of imiquimod-induced psoriasis. In this model, IL-38 knockout (IL-38 KO) mice show delayed disease resolution with exacerbated IL-17-mediated inflammation, which is reversed by the administration of mature IL-38 or γδ T cell-receptor-blocking antibodies. Mechanistically, X-linked IL-1 receptor accessory protein-like 1 (IL1RAPL1) is upregulated upon γδ T cell activation to feedforward-amplify IL-17 production and is required for IL-38 to suppress γδ T cell IL-17 production. Accordingly, psoriatic IL1RAPL1 KO mice show reduced inflammation and IL-17 production by γδ T cells. Our findings indicate a role for IL-38 in the regulation of γδ T cell activation through IL1RAPL1, with consequences for auto-inflammatory disease.

: http://publica.fraunhofer.de/dokumente/N-558713.html