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Th17细胞的研究进展

Research advance of Th17
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摘要 在不同的免疫微环境和特定的细胞因子作用下，幼稚CD4^＋T细胞会向不同的T细胞亚群分化。最初发现的两类CD4^＋T细胞亚群是Th1和Th2。Th1主要通过分泌IFN-γ等细胞因子在清除外来病原体中发挥重要作用；Th2主要通过分泌IL-4、IL-13、IL-5等细胞因子进一步激活B细胞产生抗体，并介导体液免疫。最近有新的CD4^＋T细胞亚群被发现，即分泌IL-17的CD4^＋T细胞-Th17。Th17具有强大的促炎作用，并诱导和参与了众多免疫炎症性疾病的发生。Th17细胞表面标记的寻找、分化的调控以及与自身免疫性疾病发病的关系是目前该领域研究的热点，近年在这方面的研究也取得了一定的突破。 Under distinct cytokine milieus, naive T ceils can differentiate into distinct helper T（Th） cells. Classically, Th are defined as typel （Th1） or Th2 based on the cytokine expression profiles including interferon-γ and IL-4, respectively. Through enhancing cellular immunity, Thl cells are important for the clearance of intraceUular pathogens. Th2 cells characteristically enhance humoral immunity. Th17, a subset of CD4^＋ T cells, was identified on the basis of its ability to produce IL-17. Th17 ceils play a key role as effectot cells in various settings, including inflammation and autoimmunity. Th17 cells are on the latest research centre stage of immunity. Their roles in the pathogenesis of autoimmune diseases, the transcriptional regulation and surface biomaker screening of Th17 cells are key issues to be investigated .
作者 杨骥 储以微 李明
机构地区 复旦大学中山医院皮肤科 复旦大学上海医学院免疫学系
出处 《国际免疫学杂志》 CAS 北大核心 2009年第5期375-379,共5页 International Journal of Immunology
基金 国家自然科学基金资助项目（30872274）
关键词 白细胞介素17 TH17 Interleukin-17 Th17
分类号 R392.1 [医药卫生—免疫学]
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参考文献23

  • 1Langrish CL, Chen Y, Blumenschein WM, et al. IL-23 drives a pathogenic T cell population that induces autoimmune inflammation. J Exp Med,2005,201 (2) :233-240.
  • 2Harrington LE, Hatton RD, Mangan PR, et al. Interleukin 17-producing CD4 + effector T ceils develop via a lineage distinct from the T helper type 1 and 2 lineages. Nat hnmunol,2005,6( 11 ) : 1123- 1132.
  • 3Park H, Li Z, Yang XO, Chang SH, et al. A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17. Nat hnmuno1,2005,6 ( 11 ) : 1133-1141.
  • 4Yang L, Anderson DE, Baecher-Allan C, et al. IL-21 and TGF-beta are required for differentiation of human T(H)17 cells. Nature, 2008,454(7202) :350-352.
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二级参考文献23

  • 1Lawrence Steinman A brief history of TH17, the first major revision in the TH1/TH2 hypothesis of T cell - mediated tissue damage. Nature Medicine, Review,2007,13 (2) : 139-145
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  • 3Park H, Li ZX,Yang XO, et al. A distinct lieage of CIM T cells regu latestissue Inflammation by producing interleukin 17. Nat Immunol, 2005,6( 11 ) :1133-1141
  • 4Ivanov,I. I. et al. The orphan nuclear receptor RORgammat directs the differentiation program of proinflarmnatory IL-17 + T helper cells. Cell,2006,126 : 1121-1133
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  • 6Chen Y, Langrish C L, Mckenzie B, et al. Anti-IL-23 therapy inhibits multiple inflammatory pathways and ameliorates autoimmune encephalomyelitis. J Clin Invest ,2006,116 ( 5 ) : 1317-1326
  • 7Rho J, Takami M, Choi Y, et al. Osteoimmunology : interactions of the immune and skeletal systems. J Mol Cells ,2004,17 (1) :1-9
  • 8Nakajima H, Takamori H, Hiyama Y & Tsukada W. The effect of treatment with recombinant gamma-interferon on adjuvant-induced arthritis in rats. J Agents Actions, 1991,34:63 -65
  • 9Chabaud M, Page G, Miossec P. Enhancing effect of IL-1, IL-17, and TNF-alpha on macrophage inflammatory protein-3alpha production in rheumatoid arthritis: regulation by soluble receptors and Th2 cytokines. J Immunol,2001,167 :6015-6020.
  • 10Chabaud M, Garnero P, Dayer JM, et al. Contribution of interleukin 17 to synovium matrix destructionin rheumatoid arthritis. Cytokine ,2000,12 : 1092-1099.

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国际免疫学杂志
2009年 第5期

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