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Th17细胞与Graves’病 被引量:1

Advancement of Thl7 lymphocyte in Graves' disease
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摘要 Th17细胞是近几年研究发现的一类不同于Th1和Th2细胞亚群的新型CD4^+效应T细胞。该类细胞是由天然T细胞前体分化而来,具有独立分化和发育调节机制,在其分化过程中需要IL-6和转化生长因子。B、转录因子RORα及STAT3等的参与,主要分泌IL-17A、IL-17F、IL-22等多种细胞因子,并参与多种炎症、自身免疫性疾病的发生和发展。Graves’病(GD)是一种器官特异性自身免疫病,Th2细胞介导的体液免疫在其发病中起着重要作用。近来有研究提示IL-23/Th17轴亦参与GD的发展。因此了解Th17细胞分化的影响因素、产生的细胞因子以及在免疫性疾病GD中的作用具有重要的临床意义。 Recent studies have defined a new subset of the CD4^+ T-cell effectors the Th17 lineage, which is derived from nature T cell precursor and distinct from Thl and Th2. It possesses independent regulatory mechanisms of differentiation and development. Some factors, such as the unique combination of interleukin-6 and transforming growth factor-β, Orphan nuclear receptor-γt, signal transducer and activator of transcription 3 are required for the differentiation of Th17 cell, resulting in the production of the signature cytokines interleukin-17A,IL-17F, and IL-22, etc. Th17 plays an important function in the host-defense-response, but also has become notorious for its role in the pathogenesis of many autoimmune diseases. Graves' disease (GD) is an organ-specific autoimmune disease, in the pathogenesis of which Th2 plays an important role. Recently, the IL-23/Th17 axis and its subsequent response have been found to take part in both develpment and maintenance of GD. Studying the effect factors on the differentiation of ThlT, the cytokines profiling, the function of the cell lineage involved in GD is extremely significant.
出处 《国际免疫学杂志》 CAS 北大核心 2011年第1期40-44,共5页 International Journal of Immunology
关键词 TH17细胞 分化 调节 Graves’病 Th17 cells Differentiation Regulation Graves' disease
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  • 1Bettelli E,Korn T, Kuchroo V K. Th17: the third member of the effector T cell trilogy. Curt Opin Immunol,2007,19(6) : 652-657.
  • 2Yang XO,Pappu BP,Nurieva R,et al. T helper 17 lineage differentiation is programmed by orphan nuclear receptors ROR alpha and ROR gamma. Immunity,2008,28(1) :29-39.
  • 3Fujimoto M, Serada S, Naka T. Role of IL-6 in the development and pathogenesis of CIA and EAE. Nihon Rinsho Meneki Gakkai Kaisbi,2008,31 (2) :78-84.
  • 4Veldhoen M,Hocking R J, Atkins C J, et al. TGF-β in the context of an inflammatory cytokine milieu supports de novo differentiation of IL-17-producing T cells. Immunity, 2006,24(2) :179-189.
  • 5Sutton C, Brereton C, Keogh B, et al. A crucial role for interleukin (IL)-1 in the induction of IL-17-producing T cells that mediate autoimmune encephalomyelitis. J Exp Med, 2006,203 (7) : 1685- 1691.
  • 6Shevach EM, Davidson TS, Huter EN, et al. Role of TGF-beta in the Induction of Foxp3 Expression and T Regulatory Cell Function. J Clin Immunol, 2008, Sep 23, [ Epub ahead of print].
  • 7Awasthi A, Murugaiyan G, Kuchroo VK. Interplay Between Effector Th17 and Regulatory T Cells. J Clin Immunol, 2008 , Sep 23, [ Epub ahead of print].
  • 8Mueida D, Park Y, Kim G,et al. Reciprocal TH17 and regulatory T cell differentiation mediated by retinoic acid. Science, 2007,317 (5835) :256-260.
  • 9Nakae S,Saijo S,Horai R,et al. IL-17 production from activated T cells is required for the spontaneous development of destructive arthritis in mice deficient in IL-1 receptor antagonist. Proc Natl Acad Sci USA,2003,100(10) :5986-5990.
  • 10LiangSC,TanXY,LuxenbergDP,et al. Interleukin (IL)-22 and IL-17 are eoexpressed by Th17 cells and cooperatively enhance expression of antimicrobial peptides. J Exp Med,2006,203 (10) : 2271-2279.

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  • 1Douglas RS,Naik V,Hwang CJ,et al.B cells from patients with Graves' disease aberrantly express the IGF-1 receptor:implications for disease pathogenesis[J].J Immunol,2008,181 (8):5768-5774.
  • 2Muldoon BT,Mai VQ,Burch HB.Management of Graves' Disease:An Overview and Comparison of Clinical Practice Guidelines with Actual Practice Trends[J].Endocrin Metab Clin,2014,43 (2):495-516.
  • 3Menconi F,Marcocci C,Marino M.Diagnosis and classification of Graves' disease[J].Autoimmun Rev,2014,13(4-5):398-402.
  • 4Simmonds MJ.GWAS in autoimmune thyroid disease:redefining our understanding of pathagenesis[J].Nat Rev Endocrinol,2013,9(5):277-287.
  • 5Bahn RS.Autoimmunity and Graves' disease[J].Clin Pharmacol Ther,2012,91 (4):577-579.
  • 6Klatka M,Grywalska E,Partyka M,et al.Impact of methimazole treatment on magnesium concentration and lymphocytes activation in adolescents with Graves' disease[J].Biol Trace Elem Res,2013,153(1-3):155-170.
  • 7Van der Weerd K,Van Hagen PM,Schrijver B,et al.The peripheral blood compartment in patients with Graves' disease:activated T lymphocytes and increased transitional and pre-naive mature B lymphocytes[J].Clin Exp Immunol,2013,174 (2):256-264.
  • 8Browning JL.B cells move to centre stage:novel opportunities for autoimmune disease treatment[J].Nat Rev Drug Discov,2006,5 (7):564-576.
  • 9Renaudineau Y,Garaud S,Le Dantec C,et al.Autoreactive B cells and epigenetics[J].Clin Rev Allergy Immunol,2010,39 (1):85-94.
  • 10Chen CR,Pichurin P,Nagayama Y,et al.The thyrotropin receptor autoantigen in Graves disease is the culprit as well as the victim[J].J Clin Invest,2003,111 (12):1897-1904.

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