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Ⅰ型糖尿病是T细胞介导的自身免疫性疾病,Th细胞亚群在疾病的发生过程中起了一定的作用。其中致病性免疫过程是由T细胞亚群Th1介导的,而TH2细胞亚群则是介导保护性免疫反应的。Th1型细胞因子(IL-2.IFN)通过直接促进细胞凋亡和/或上调选择性粘附分子的表达,以及Th1细胞因子可促进自身反应性T细胞在胰腺的浸润,二者均导致β细胞的破坏;Th1细胞介导的针对谷氨酸脱羧酶(GAD)的自身免疫反应增强,并通过分子内和分子间传导的机制转导至其他β细胞。Th1和Th2亚群实质上是机体在特异性抗原刺激下,Th细胞发生相对优势转化的结果。Th细胞的优势转化具有可塑性,对Th1或Th2型细胞因子或抗细胞因子单抗的研究,将为临床上自身免疫性糖尿病的治疗开辟新的途径。
Type I diabetes is a T-cell mediated autoimmune disease and the Th cell subset plays a role in the pathogenesis of the disease. Among them, the pathogenic immune process is mediated by the T cell subsets Th1, while the TH2 cell subsets mediate the protective immune response. Th1-type cytokines (IL-2.IFN) both promote the expression of beta-cell adhesion molecules by directly stimulating apoptosis and / or up-regulating the expression of selective adhesion molecules, and Th1 cytokines promote the infiltration of autoreactive T cells in the pancreas, Cell destruction; Th1 cell-mediated autoimmune responses to glutamate decarboxylase (GAD) are enhanced and transduced to other beta cells via intramolecular and intermolecular transduction mechanisms. The Th1 and Th2 subsets are essentially the result of a relatively dominant transformation of Th cells under the stimulation of specific antigens. The predominant transformation of Th cells is plastic. The study of Th1 or Th2-type cytokines or anti-cytokine monoclonal antibodies will open up new avenues for the clinical treatment of autoimmune diabetes.