IL-17: A new actor in IFN-driven systemic autoimmune diseases

被引:65
作者
Ambrosi, Aurelie [1 ]
Espinosa, Alexander [2 ]
Wahren-Herlenius, Marie [1 ]
机构
[1] Karolinska Hosp, Rheumatol Unit, Dept Med, Karolinska Inst,Ctr Mol Med, S-17176 Stockholm, Sweden
[2] Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA
基金
瑞典研究理事会;
关键词
IFN; IL-17; systemic autoimmune disease; systemic lupus erythematosus; Th17; TOLL-LIKE RECEPTORS; T-HELPER-CELLS; INTERLEUKIN; 23; RECEPTOR; MALIGNANT CARCINOID-TUMORS; ALPHA MONOCLONAL-ANTIBODY; ZEALAND BLACK MICE; LUPUS-ERYTHEMATOSUS; INTERFERON-ALPHA; TH17; CELLS; SJOGRENS-SYNDROME;
D O I
10.1002/eji.201242653
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Systemic autoimmune diseases such as systemic lupus erythematosus are type I IFN-driven diseases with exaggerated B-cell responses and autoantibody production. Th17 cells, a T-helper-cell subset with high inflammatory capacity, was initially discovered and characterized in the context of experimental autoimmune encephalomyelitis an animal model of multiple sclerosis. There is now emerging evidence that Th17 cells, and more generally IL-17 and IL-17-producing cells, may play a role in the pathogenesis of type I IFN-driven systemic autoimmune diseases such as lupus. Here, we review the different studies suggesting a role for IL-17 and IL-17-producing cells in systemic autoimmune diseases, both in humans and in animal models, and we consider the possible mechanisms by which these cells may contribute to disease. We also discuss the hypothesis that type I IFN and IL-17 act in concert to sustain and amplify autoimmune and inflammatory responses, making them a dangerous combination involved in the pathogenesis of systemic autoimmune diseases.
引用
收藏
页码:2274 / 2284
页数:11
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