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多发性硬化免疫机制研究新进展 被引量:2

Resent progression of researches on the immune mechanism of multiple sclerosis
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摘要 多发性硬化(MS)是一种以中枢神经系统白质神经变性为特征的自身免疫性疾病,其确切的病因发病机制尚不清楚。目前认为是在易感基因的基础上,受环境因素的触发由CD4^+T细胞介导的中枢神经系统的自身免疫性疾病,但其他免疫细胞(包括B细胞、CD8^+T细胞等)也能通过诱导或调控MS患者中枢神经系统内的免疫应答过程而可能参与MS的发病。以往认为Th1/Th2型反应失衡是其关键致病因素,近年来随着对其研究的深入,提出许多新的观点,为多发性硬化的免疫机制及治疗策略研究提供了新方向。 Multiple sclerosis (MS) is a kind of autoimmune diseases. It is characterized by neural degeneration in white matter of central nervous system. Its etiological factor and pathogenesis are unclear. It is believed that the main pathogenesis factor of MS is the unbalance of Th1/Th2 immunoreaction, while other immunocytes, such as CD8^+ T cells, B lymphocytes, and innate immune factors also take part in its pathopoiesis. Reacently some novel ideas are proposed through intensive reseaches. Particular interest is currently focused on a distinct lineage of T cells that specialize in IL-17 production (Th17) which exerts a pathogenesis role in EAE. It has been proposed that the activity of regulatory CD4 + CD25^+ Foxp3^+ T cells ameliorates the clinical symptoms of EAE and restrain the progress of the disease in several animal models. It provides new insight for the study of the immune mechanism and the developonent treatment strategies of MS.
作者 侯娟
出处 《国际免疫学杂志》 CAS 北大核心 2009年第6期468-471,共4页 International Journal of Immunology
关键词 多发性硬化 感染损伤 T细胞 B细胞 固有免疫 Multiple sclerosis Infection and damage T ceils B cells Innate immunity
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参考文献21

  • 1Steinman L. Nuanced roles of cytokines in three major human brain disorders. J Clin Invest,2008,118 ( 11 ) :3557-3563.
  • 2Steinman L. A brief history of T(H) 17, the first major revision in the T(H) I/T (H) 2 hypothesis of T cell-mediated tissue damage. Nat Meal,2007,13 (2) : 139-145.
  • 3Tzartos JS, Friese MA, Craner M J, et al. Interleukin-17 production in central nervous system-infiltrating T cells and glial cells is associated with active disease in muhiple sclerosis. Am J Pathol,2008, 172(1 ) :146-155.
  • 4Kebir H, Kreymborg K, Ifergan I, et al. Human TH17 lymphocytes promote blood-brain barrier disruption and central nervous system inflammation. Nat Med ,2007,13 (10) : 1173-1175.
  • 5吴学忠.Th17细胞的研究进展[J].国际免疫学杂志,2007,30(6):428-432. 被引量:7
  • 6Kroenke MA, Carlson TJ, Andjelkovic AV, et al. IL-12- and IL- 23-modulated T cells induce distinct types of EAE based on histology, CNS chemokine profile, and response to cytokine inhibition. J Exp Med ,2008,205 ( 7 ) : 1535-1541.
  • 7Martin-Saavedra FM, Flores N, Dorado B, et al. Beta-interferon unbalances the peripheral T cell proinflammatory response in experimental autoimmune encephalomyelitis. Mol Immunol, 2007, 44 (14) :3597-3607.
  • 8Martin-Saavedra FM, Gonzalez-Gareia C, Bravo B, et al. Beta interferon restricts the inflammatory potential of CD4 + cells through tile boost of the Th2 phenotype, the inhibition of Th17 response and the prevalence of naturally oeeurring T regulatory cells. Mol Immunol,2008,45 ( 15 ) :4008-4019.
  • 9Shinohara ML, Kim JH, Garcia VA, et al. Engagement of the type I interferon receptor on dendritic cells inhibits T helper 17 cell development: role of intracellular osteopontin. Immunity, 2008,29 ( 1 ) :68-78.
  • 10Guo B, Chang EY, Cheng G. The type I IFN induction pathway constrains ThlT-mediated autoimmune inflammation in mice. J Clin Invest ,2008,118 ( 5 ) : 1680-1690.

二级参考文献31

  • 1冯晓明,韩忠朝.IL-27在Th1型免疫发生中的作用[J].国际免疫学杂志,2006,29(5):277-282. 被引量:2
  • 2Bettelli E ,Sullivan B ,Szabo SJ, et al. Loss of T-bet, but not STAT1, prevents the development of experimental autoimmune encephalomyelitis. J Exp Med, 2004,200( 1 ):79-87.
  • 3Murphy CA, Langrish CL, Chen Y, et al. Divergent pro- and anti-inflammatory roles for IL-23 and IL-12 in joint autoimmune inflammation. J Exp Med,2003,198(12) :1951-1957.
  • 4Zhang GX, Gran B, Yu S, et al. Induction of experimental autoimmune encephalomyelitis in IL-12 receptor-beta 2-deficient mice: IL-12 responsiveness is not required in the pathogenesis of inflammatory demyelination in the central nervous system. J Immunol, 2003,170 (4) : 2153-2160.
  • 5Aggarwal S,Ghilardi N,Xie MH,et al. Interleukin-23 promotes a distinct CD4 T cell activation state characterized by the production of interleukin-17. J Biol Chem ,2003, 278 ( 3 ) : 1910-1914.
  • 6Nakae S,Nambu A,Sudo K,et al. Suppression of immune induction of collagen-induced arthritis in IL-17-deficient mice. J Immunol,2003, 171 ( 11 ) :6173-6177.
  • 7Lubberts E,Joosten LA,Oppers B,et al. IL-1-independent role of IL-17 in synovial inflammation and joint destruction during collagen-induced arthritis. J Immunol,2001, 167(2) :1004-1013.
  • 8Koenders MI,Lubberts E,Oppers-Walgreen B ,et al. Induction of cartilage damage by overexpression of T cell interletrkin-17A in experimental arthritis inmice deficient in interleukin-1. Arthritis Rheum, 2005,52 ( 3 ) :975-983.
  • 9Bettelli E,Kuchroo VK. IL-12- and IL-23-induced T helper cell subsets: birds of the same feather flock together. J Exp Med,2005,201 (2) :169-171.
  • 10Langrish 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.

共引文献8

同被引文献12

  • 1尉杰忠,孙永胜,马存根(审校),梁丽云(审校),米亚英(审校).细胞因子在实验性自身免疫性脑脊髓炎耐受中的作用[J].国际免疫学杂志,2006,29(3):160-164. 被引量:8
  • 2Imitola J, Chitnis T, Khoury SJ. Cytokines in multiple sclerosis: from bench to bedside[J]. Pharmacol Ther, 2005,106(2) : 163 - 177.
  • 3Centonze D, Bad M, Rossi S, et al. The endocannabinoid system is dysregulated in multiple sclerosis and in experimental autoimmune encephalo- myelitis [ J]. Brain, 2007,130 : 2543 - 2553.
  • 4Brueklacher-Waldert V, Stueruer K, KolsterM, et al. Phenotypical and functional characterization of T helper 17 cells in multiple sclerosis [J]. Brain, 2009, 132 (12) : 3329 -3341.
  • 5Dardalhon V, Konr T, Kuehroo VK, et al. Role of Thl and Thl7 ceils in prgan--specific autoimmunity [ J ]. Autoimmun, 2008,31 ( 3 ) : 252 - 256.
  • 6Fowler CJ, Rojo ML, Rodriguez-Gaztelumendi A. Modulation of the endocannabinoid system: neuropro- tection or neurotoxicity? [ J]. Exp Neurol, 2010,224 (1) : 37 -47.
  • 7Rossi S, Bernardi G, Centonze D. The endocannab- inoid system in the inflammatory and neurodegenerative processes of multiple sclerosis and of amyotrophic lateral sclerosis[J]. Exp Neurol, 2010,224( 1 ) : 92 - 102.
  • 8林琳,杨丹,付锦.Th1细胞和Th17细胞在多发性硬化和实验性变态反应性脑脊髓炎发生中的作用[J].国际免疫学杂志,2012,35(1):5-8. 被引量:5
  • 9周建光,杨梅,华川.IL-10与自身免疫性疾病关系的研究进展[J].医学综述,2012,18(17):2743-2745. 被引量:11
  • 10徐雁.多发性硬化的生物学标记物[J].中国神经免疫学和神经病学杂志,2013,20(2):82-84. 被引量:5

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