Interleukin 31, a cytokine produced by activated T cells, induces dermatitis in mice

被引:834
作者
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
机构
[1] Zymogenet Inc, Dept Immunol, Seattle, WA 98102 USA
[2] Zymogenet Inc, Dept Cytokine Biol, Seattle, WA 98102 USA
[3] Zymogenet Inc, Dept Preclin Dev, Seattle, WA 98102 USA
[4] Zymogenet Inc, Dept Comp Sci, Seattle, WA 98102 USA
[5] Zymogenet Inc, Dept Genet, Seattle, WA 98102 USA
[6] Zymogenet Inc, Dept Prot Biochem, Seattle, WA 98102 USA
[7] Zymogenet Inc, Dept In Vitro Biol, Seattle, WA 98102 USA
关键词
D O I
10.1038/ni1084
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 [免疫学];
摘要
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 expressed both mRNAs constitutively. Transgenic mice overexpressing IL-31 developed severe pruritis, 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.
引用
收藏
页码:752 / 760
页数:9
相关论文
共 37 条
[1]
T cells and T cell-derived cytokines as pathogenic factors in the nonallergic form of atopic dermatitis [J].
Akdis, CA ;
Akdis, M ;
Simon, D ;
Dibbert, B ;
Weber, M ;
Gratzl, S ;
Kreyden, O ;
Disch, R ;
Wüthrich, B ;
Blaser, K ;
Simon, HU .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 1999, 113 (04) :628-634
[2]
Molecular phylogeny within type I cytokines and their cognate receptors [J].
Boulay, JL ;
O'Shea, JJ ;
Paul, WE .
IMMUNITY, 2003, 19 (02) :159-163
[3]
Expression of interleukin-4 in the epidermis of transgenic mice results in a pruritic inflammatory skin disease: An experimental animal model to study atopic dermatitis [J].
Chan, LS ;
Robinson, N ;
Xu, LT .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 2001, 117 (04) :977-983
[4]
Gene microarrays reveal extensive differential gene expression in both CD4+ and CD8+ type 1 and type 2 T cells [J].
Chtanova, T ;
Kemp, RA ;
Sutherland, APR ;
Ronchese, F ;
Mackay, CR .
JOURNAL OF IMMUNOLOGY, 2001, 167 (06) :3057-3063
[5]
Isolation and primary culture of murine alveolar type II cells [J].
Corti, M ;
Brody, AR ;
Harrison, JH .
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 1996, 14 (04) :309-315
[6]
Toll-like receptor 4 is required for optimal development of Th2 immune responses: Role of dendritic cells [J].
Dabbagh, K ;
Dahl, ME ;
Stepick-Biek, P ;
Lewis, DB .
JOURNAL OF IMMUNOLOGY, 2002, 168 (09) :4524-4530
[7]
GPL, a novel cytokine receptor related to GP130 and leukemia inhibitory factor receptor [J].
Diveu, C ;
Lelièvre, E ;
Perret, D ;
Lak-Hal, AHL ;
Froger, J ;
Guillet, C ;
Chevalier, S ;
Rousseau, F ;
Wesa, A ;
Preissner, L ;
Chabbert, M ;
Gauchat, JF ;
Galy, A ;
Gascan, H ;
Morel, A .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (50) :49850-49859
[8]
Lipopolysaccharide-enhanced, toll-like receptor 4-dependent T helper cell type 2 responses to inhaled antigen [J].
Eisenbarth, SC ;
Piggott, DA ;
Huleatt, JW ;
Visintin, I ;
Herrick, CA ;
Bottomly, K .
JOURNAL OF EXPERIMENTAL MEDICINE, 2002, 196 (12) :1645-1651
[9]
A novel type I cytokine receptor is expressed on monocytes, signals proliferation, and activates STAT-3 and STAT-5 [J].
Ghilardi, N ;
Li, J ;
Hongo, JA ;
Yi, S ;
Gurney, A ;
de Sauvage, FJ .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (19) :16831-16836
[10]
TACI and BCMA are receptors for a TNF homologue implicated in B-cell autoimmune disease [J].
Gross, JA ;
Johnston, J ;
Mudri, S ;
Enselman, R ;
Dillon, SR ;
Madden, K ;
Xu, WF ;
Parrish-Novak, J ;
Foster, D ;
Lofton-Day, C ;
Moore, M ;
Littau, A ;
Grossman, A ;
Haugen, H ;
Foley, K ;
Blumberg, H ;
Harrison, K ;
Kindsvogel, W ;
Clegg, CH .
NATURE, 2000, 404 (6781) :995-999