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首页> 外文期刊>Nature immunology >Recessive tolerance to preproinsulin 2 reduces but does not abolish type 1 diabetes.
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Recessive tolerance to preproinsulin 2 reduces but does not abolish type 1 diabetes.

机译：对胰岛素原2的隐性耐受性降低但不会消除1型糖尿病。

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摘要

Although autoimmune diseases can be initiated by immunization with a single antigen, it is not clear whether a single self antigen is essential for the initiation and, perhaps, the perpetuation of spontaneous autoimmunity. Some studies have suggested that insulin may represent an essential autoantigen in type 1 diabetes. Here we show that unlike tolerance to glutamic acid decarboxylase, tolerance to transgenically overexpressed preproinsulin 2 substantially reduced the onset and severity of type 1 diabetes in nonobese diabetic mice. However, some mice still developed type 1 diabetes, suggesting that insulin is a key, but not absolutely essential, autoantigen. The results are consistent with the idea that the human IDDM2 locus controls susceptibility to type 1 diabetes by regulating intrathymic preproinsulin expression.
机译：尽管自身免疫性疾病可以通过单一抗原免疫来引发，但尚不清楚单个自身抗原是否对启动以及自发性自身免疫永续性至关重要。一些研究表明，胰岛素可能是1型糖尿病中必不可少的自身抗原。在这里，我们显示出与对谷氨酸脱羧酶的耐受性不同，对转基因过度表达的胰岛素原2的耐受性显着降低了非肥胖糖尿病小鼠中1型糖尿病的发作和严重程度。但是，一些小鼠仍患有1型糖尿病，这表明胰岛素是关键的但不是绝对必要的自身抗原。该结果与人类IDDM2基因座通过调节胸腺内胰岛素原的表达来控制1型糖尿病的敏感性相一致。

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