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HLA‐DR3 mediated CD4 T cell response against GAD65 in type 1 diabetes patients
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HLA‐DR3 mediated CD4 T cell response against GAD65 in type 1 diabetes patients
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Journal Article
HLA‐DR3 mediated CD4 T cell response against GAD65 in type 1 diabetes patients
2023
Overview
目的:我们进行这项研究以确定与1型糖尿病(T1D)中人类白细胞抗原(HLA)‐DR3/DQ2介导的谷氨酸脱羧酶(GAD65)特异性CD4 T细胞激活可能相关的致糖尿病性GAD65肽。 方法:选取与HLA‐DR3/DQ2分子在体外结合强烈的前30个GAD65肽, 分为4个池组。使用这些肽来刺激研究对象的CD4 T细胞, 在16小时PBMC培养中分析CD4 T细胞对干扰素(IFN‐γ), 白介素(IL)‐17, 肿瘤坏死因子‐α(TNF‐α)和IL‐10的激活表达, 使用流式细胞术进行分析。 结果:所有四个GAD65肽池(PP1‐4)都导致CD4 T细胞的IFN‐γ表达明显增加(p=0.003, p<0.0001, p=0.026 和 p=0.002, 分别), 只有池2在T1D患者与健康对照组之间显示出显著的IL‐17表达增加(p<0.0001)。肽间组间比较显示, 在患者中, PP2组与其他组相比, IFN‐γ和IL‐17的表达显著增加, IL‐10的表达显著降低(p<0.0001, p=0.02 和 p=0.04), 但在对照组中没有显示出明显差异。此外, 2号组肽对于HLA‐DRB1 * 03‐DQA1 * 05‐DQB1 * 02 + 患者而言, 导致CD4 T细胞的IFN‐γ和IL‐17表达显著增加(p=0.002), 而IL‐10表达显著降低(p=0.04)。在HLA‐DRB1 * 03‐DQA1 * 05‐DQB1 * 02 +的最近诊断的T1D患者中, CD4 T细胞的IL‐17表达显著增加(p=0.03)。 结论:GAD65肽, 尤其是属于PP2的肽段, 在T1D患者中能够诱导CD4 T细胞表达IFN‐γ和IL‐17细胞因子, 这表明在患者中2号组肽可能通过HLA‐DR3分子递呈给CD4 T细胞, 使免疫平衡朝向炎症表型转变。
Publisher
John Wiley & Sons, Inc,Wiley Publishing Asia Pty Ltd
Subject
