Nat. Immunol. 2004 Jul
Dillon SR, Sprecher C, Hammond A, Bilsborough J, Rosenfeld-Franklin M, Presnell SR, Haugen HS, Maurer M, Harder B, Johnston J, Bort S, Mudri S, Kuijper JL, Bukowski T, Shea P, Dong DL, Dasovich M, Grant FJ, Lockwood L, Levin SD, LeCiel C, Waggie K, Day H, Topouzis S, Kramer J, Kuestner R, Chen Z, Foster D, Parrish-Novak J, Gross JA
Abstract
T cell-derived cytokines are important in the development of an effective immune response, but when dysregulated they can promote disease. Here we identify a four-helix bundle cytokine we have called interleukin 31 (IL-31), which is preferentially produced by T helper type 2 cells. IL-31 signals through a receptor composed of IL-31 receptor A and oncostatin M receptor. Expression of IL-31 receptor A and oncostatin M receptor mRNA was induced in activated monocytes, whereas epithelial cells expre
...[more]ssed both mRNAs constitutively. Transgenic mice overexpressing IL-31 developed severe pruritus, alopecia and skin lesions. Furthermore, IL-31 receptor expression was increased in diseased tissues derived from an animal model of airway hypersensitivity. These data indicate that IL-31 may be involved in promoting the dermatitis and epithelial responses that characterize allergic and non-allergic diseases.
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Mesh Headings:
Amino Acid Sequence, Animals, Dermatitis, Flow Cytometry, Gene Deletion, Gene Expression Profiling, Humans, Hypersensitivity, Infusion Pumps, Implantable, Interleukins, Lung, Lymphocyte Activation, Mice, Mice, Knockout, Mice, Transgenic, Molecular Sequence Data, Polymerase Chain Reaction, RNA, Messenger, Receptors, Cytokine, Receptors, Interleukin, Receptors, Oncostatin M, T-Lymphocytes, Transgenes, Up-Regulation