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.
journal_name
Cell Repjournal_title
Cell reportsauthors
Han Y,Mora J,Huard A,da Silva P,Wiechmann S,Putyrski M,Schuster C,Elwakeel E,Lang G,Scholz A,Scholz T,Schmid T,de Bruin N,Billuart P,Sala C,Burkhardt H,Parnham MJ,Ernst A,Brüne B,Weigert Adoi
10.1016/j.celrep.2019.03.082subject
Has Abstractpub_date
2019-04-16 00:00:00pages
835-846.e5issue
3issn
2211-1247pii
S2211-1247(19)30421-8journal_volume
27pub_type
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