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Th17与自身免疫性疾病 被引量:2

Th17 and autoimmune diseases
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摘要 当初始CD4^+T细胞接受抗原刺激时,在不同的细胞因子环境中分化为不同的淋巴细胞亚群。Th17作为一种额的T细胞亚群是在TGF-β与IL-6存在时经由孤独核受体(ROR)-γt途径分化而来,而当环境中仅有TGF-β时却分化为CD4^+CD25^+Foxp3^+调节性T细胞(Tr)。与Th1一样,Th17被认为在自身免疫性疾病和炎症反应的发生和进展中都发挥重要的病理作用,相反,Tr则起着抗炎和免疫负性调节的作用。因此Th1及Th17倾向的免疫应答可能导致炎症反应与自身免疫性疾病的发生和进展,故在体内阻断其相关的细胞因子IL-17、IL-6等则可使Th1、Th17及Tr重新保持平衡而对自身免疫性疾病产生治疗作用。 naive CD4^+ T helper cells can be induced to differentiate towards different subsets according to the local cytokine milieu. When the growth factor (TGF)-β and IL-6 are present, naive CD4^+ T helper ceils always differentiate into Th17 a new T cell subset which is characterized by the expression of specific transcription factor orphan nuclear receptor (ROR) -γt. There is considerable evidence for the importance of Th17 in the development and progression of inflammatory and autoimmune diseases. In contrast, CD4^+ CD25^+ Foxp3^+ regulatory T cells(Treg) have anti-inflammatory properties and can cause quiescence of autoimmune diseases. As a result, it can be proposed that the immune response towards Th17 or Thl may be responsible for the development and progression of inflammatory and autoimmune diseases in humans. Blocking critical cytokines in vivo such as IL-17,IL-6 may result in a new balance between Th1 ,Th17 and Treg,which will induce the quiescence of inflammatory and autoimmune diseases.
出处 《国际免疫学杂志》 CAS 2008年第5期389-393,共5页 International Journal of Immunology
关键词 TH17 IL-17 自身免疫性疾病 Th17 Interleukin-17 Autoimmune diseases
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同被引文献37

  • 1Conti H R, Shen F, Nayyar N.Thl7 cells and IL-17 receptor signaling are essential for mucosal host defense against oral candidiasis[J]. J Exp Med, 2009, 206(2):299-311.
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  • 9Sato K, Suematsu A, Okamoto K. TH17 functions as an osteoclastogenic helper T cell subset that links T cell activa- tion and bone destruction[J]. J Exp Med, 2006, 203(12): 2673-2682.
  • 10Conti H R, Shen F, Nayyar N. TH17 cells and IL-17 receptor signaling are essential for mucosal host defense against oral candidiasis[J]. J Exp Med, 2009, 206(2):299-311.

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