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Immune modulation for prevention of type 1 diabetes mellitus.

机译:免疫调节可预防1型糖尿病。

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Prevention of type 1 diabetes mellitus requires early intervention in the autoimmune process directed against beta cells of the pancreatic islets of Langerhans. This autoimmune inflammatory process is thought to be caused by the effect of Th1 cells and their secreted cytokines (e.g. interferon) and to be suppressed by Th2-secreted anti-inflammatory cytokines (e.g. IL-4, IL-10). Various methods aimed specifically at halting or modulating this response have been attempted. An alternative method is the re-induction of tolerance towards the putative self antigen that causes the disease. Proposed antigens such as insulin, glutamic acid decarboxilase (GAD) and the heat shock protein 60 (Hsp60)-derived peptide 277 have been used successfully in murine diabetes models and in initial clinical trials in early diabetes patients. Here, we review the results of these trials.
机译:预防1型糖尿病需要及早干预针对Langerhans胰岛β细胞的自身免疫过程。这种自身免疫性炎症过程被认为是由Th1细胞及其分泌的细胞因子(例如干扰素)的作用引起的,并被Th2分泌的抗炎细胞因子(例如IL-4,IL-10)抑制。已经尝试了各种旨在中止或调节该反应的方法。一种替代方法是重新诱导对引起该疾病的推定自身抗原的耐受性。提议的抗原,例如胰岛素,谷氨酸脱羧酶(GAD)和热休克蛋白60(Hsp60)衍生的肽277已成功用于鼠类糖尿病模型和早期糖尿病患者的初步临床试验中。在这里,我们回顾了这些试验的结果。

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