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MHC class II polymorphism and central tolerance in autoimmune diabetes.

機(jī)譯：MHC II類多態(tài)性和自身免疫性糖尿病的中樞耐受性。

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Insulin-dependent diabetes mellitus is a complex disease characterized by the destruction of the pancreatic beta cells which produce insulin. A strong genetic link exist between autoimmunity and MHC class II polymorphism where different alleles infer either susceptibility or resistance from disease. The NOD mouse spontaneously develops IDDM and therefore provides an appropriate genetic background with which to study this disease. Previously it has been shown that T cells bearing an I-Ag7-restricted, beta cell reactive, highly diabetogenic T cell receptor (4.1-TCR) underwent negative selection when non-NOD MHC class II molecules were expressed in the 4.1-NOD background. Here it is shown that when 4.1-thymocytes interact with I-Ad, I-Ag7PD, or I-Eαk MHC class II molecules (expressed as transgenes) they undergo different levels of tolerance. Therefore, anti-diabetogenic MHC class II molecules may provide protection from disease by having a tolerogenic affect on highly pathogenic, 4.1-like CD4+ T cells.
機(jī)譯：胰島素依賴性糖尿病是一種復(fù)雜的疾病，其特征是破壞了產(chǎn)生胰島素的胰島β細(xì)胞。自身免疫與MHC II類多態(tài)性之間存在很強(qiáng)的遺傳聯(lián)系，其中不同的等位基因可推斷出對疾病的敏感性或耐藥性。 NOD小鼠自發(fā)形成IDDM，因此提供了研究該疾病的適當(dāng)遺傳背景。以前已經(jīng)顯示，當(dāng)在非NOD MHC II類分子中表達(dá)IA g7 限制，β細(xì)胞反應(yīng)性，高糖尿病性T細(xì)胞受體（4.1-TCR）時(shí)，T細(xì)胞會(huì)進(jìn)行陰性選擇。 4.1點(diǎn)背景。此處顯示當(dāng)4.1胸腺細(xì)胞與IA d ，IA g7PD 或I-Eα k MHC II類分子相互作用時(shí)（表示為轉(zhuǎn)基因），它們會(huì)經(jīng)歷不同程度的耐受性。因此，抗糖尿病的MHC II類分子通過對高致病性的4.1樣CD4 + T細(xì)胞產(chǎn)生致耐受作用，可以提供抗疾病的保護(hù)。

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