The roles of IL-17A in inflammatory immune responses and host defense against pathogens

被引:395
作者
Iwakura, Yoichiro [1 ]
Nakae, Susumu [2 ]
Saijo, Shinobu
Ishigame, Harumichi
机构
[1] Univ Tokyo, Inst Med Sci, Ctr Med Expt, Minato Ku, Tokyo 1088639, Japan
[2] Univ Tokyo, Inst Med Sci, Frontier Res Initiat, Tokyo 1088639, Japan
基金
日本学术振兴会;
关键词
IL-17A; IL-1; inflammation; allergic disease; autoimmune disease; bacterial infection;
D O I
10.1111/j.1600-065X.2008.00699.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
T-helper 17 (Th17) cells are a newly discovered CD4(+) helper T-cell subset that produces interleukin-17A (IL-17A) and IL-17F. IL-17A plays important roles in allergic responses such as delayed-type hypersensitivity, contact hypersensitivity, and allergic airway inflammation. IL-17A promotes inflammation by inducing various proinflammatory cytokines and chemokines, recruiting neutrophils, enhancing antibody production, and activating T cells. IL-17A expression is also augmented in autoimmune diseases such as multiple sclerosis and rheumatoid arthritis. Using mouse models of these diseases, we found that IL-17A plays a central role in their development. IL-6 is required for the development of Th17 cells and tumor necrosis factor functions downstream of IL-17A during the effector phase. IL-1 is important both for developing Th17 cells and eliciting inflammation. Th17 cells, like Th1 and Th2 cells, are involved in host defense against infections, but the contribution of these Th subsets to defense mechanisms differs among pathogens. The roles of IL-17F remain largely unknown. In this review, we introduce how IL-17A/IL-17F are involved in inflammatory immune responses and host defense mechanisms and discuss their relationship with other cytokines in the development of inflammatory and infectious diseases.
引用
收藏
页码:57 / 79
页数:23
相关论文
共 299 条
  • [21] A selective role for the TNF p55 receptor in autocrine signaling following IFN-γ stimulation in experimental autoimmune uveoretinitis
    Calder, CJ
    Nicholson, LB
    Dick, AD
    [J]. JOURNAL OF IMMUNOLOGY, 2005, 175 (10) : 6286 - 6293
  • [22] Chabaud M, 1998, J IMMUNOL, V161, P409
  • [23] Airway remodeling-associated mediators in moderate to severe asthma:: Effect of steroids on TGF-β, IL-11, IL-17, and type I and type III collagen expression
    Chakir, J
    Shannon, J
    Molet, S
    Fukakusa, M
    Elias, J
    Laviolette, M
    Boulet, LP
    Hamid, Q
    [J]. JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 2003, 111 (06) : 1293 - 1298
  • [24] Act1 adaptor protein is an immediate and essential signaling component of interleukin-17 receptor
    Chang, Seon Hee
    Park, Heon
    Dong, Chen
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2006, 281 (47) : 35603 - 35607
  • [25] CHARTERIS DG, 1992, IMMUNOLOGY, V75, P463
  • [26] Stimulation of airway mucin gene expression by interleukin (IL)-17 through IL-6 paracrine/autocrine loop
    Chen, Y
    Thai, P
    Zhao, YH
    Ho, YS
    DeSouza, MM
    Wu, R
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (19) : 17036 - 17043
  • [27] CHER DJ, 1987, J IMMUNOL, V138, P3688
  • [28] STAT3 and NF-κB signal pathway is required for IL-23-mediated IL-17 production in spontaneous arthritis animal model IL-1 receptor antagonist-deficient mice
    Cho, Mi-La
    Kang, Jung-Won
    Moon, Young-Mee
    Nam, Hyo-Jung
    Jhun, Joo-Yeon
    Heo, Seong-Beom
    Jin, Hyun-Tak
    Min, So-Youn
    Ju, Ji-Hyeon
    Park, Kyung-Su
    Cho, Young-Gyu
    Yoon, Chong-Hyeon
    Park, Sung-Hwan
    Sung, Young-Chul
    Kim, Ho-Youn
    [J]. JOURNAL OF IMMUNOLOGY, 2006, 176 (09) : 5652 - 5661
  • [29] DISSEMINATED TUBERCULOSIS IN INTERFERON-GAMMA GENE-DISRUPTED MICE
    COOPER, AM
    DALTON, DK
    STEWART, TA
    GRIFFIN, JP
    RUSSELL, DG
    ORME, IM
    [J]. JOURNAL OF EXPERIMENTAL MEDICINE, 1993, 178 (06) : 2243 - 2247
  • [30] Cutting edge: IL-21 is not essential for Th17 differentiation or experimental autoimmune encephalomyelitis
    Coquet, Jonathan M.
    Chakravarti, Sumone
    Smyth, Mark J.
    Godfrey, Dale I.
    [J]. JOURNAL OF IMMUNOLOGY, 2008, 180 (11) : 7097 - 7101