Science Immunology:重更类风湿关节炎免疫反应新认知

2021-04-21 Viho MedSci原创

类风湿性关节炎(RA)是一种自身免疫性疾病,其特点是关节肿胀、疼痛、僵硬,进而限制患者的行动能力。

莫纳什大学

类风湿性关节炎(RA)是一种自身免疫性疾病,其特点是关节肿胀、疼痛、僵硬,进而限制患者的行动能力。

HLA基因座是人类基因组中最多态的区域,使HLA分子呈现出广泛的肽段。加上多样化的T细胞库,这使得T细胞介导的适应性免疫反应能够将无数自身肽与非自身肽区分开。尽管HLA在保护性免疫中起关键作用,但某些HLA等位基因,尤其是由HLA II基因座编码的等位基因,经常与异常的T细胞免疫相关,包括自身免疫和其他免疫介导的炎症性疾病。例如,HLA-DR4同种异体与RA的易感性增加有关。但是,在许多情况下,HLA,自身抗原和最终导致T细胞自身免疫的应答性T细胞库之间的关系仍然不清楚。

T细胞耐受性的破坏可归因于多种机制,包括异常的T细胞受体(TCR-HLA对接拓扑,与HLA分子结合的肽改变,分子模拟和新表位的产生。例如,某些翻译后修饰(PTM),例如谷氨酰胺脱酰胺,肽反式剪接和瓜氨酸化,会产生新表位,其与给定的HLA分子的结合性得到改善。但是,尚未证明TCR是否可以直接识别此类PTM

近日,莫纳什大学生物医学研究所的研究团队在与RA发展相关的高危免疫基因所起的作用方面取得了突破性进展。这项长达7年的研究结果发表在Science Immunology上。

众所周知,人体白细胞抗原(HLA)-DR4会增加RA的易感性。表达HLA-DR4的个体带有共同的易感性表位(SE),增加患RA的风险。自身蛋白的翻译后修饰通过瓜氨酸化作用形成可由HLA-DR4 SE异构体呈现的新抗原。然而,在T细胞介导的自身免疫中,HLA分子、翻译后修饰的表位(s)和响应的T细胞剧目之间的相互作用仍不清楚。

在这项研究中,研究小组利用转基因小鼠表达人类HLA-DR4分子,在分子和细胞水平上研究了T细胞如何识别这些HLA-DR4分子。研究确定T细胞受体和与HLA-DR4结合的改变的关节蛋白相互作用过程中形成的分子复合物的结构。

研究发现,HLA-DR4转基因小鼠中,因从免疫前程序中选择性克隆扩张,用 Fibβ-74cit69-81 肽免疫可导致HLA-DR4 双瓜氨酸表位( Fibβ-74cit69-81)四聚体表现出偏向性的T细胞受体(TCR)β链用法的T细胞。HLA-DR4的SE具有双重功能,即表现TCR识别决定因素。

研究表明,高度相似的T细胞受体,可能具有相似的识别特征,也存在于表达HLA分子的“RA易感”人群中。

PMHCⅡ界面TCR点突变的影响

该研究通过研究T细胞如何识别与“易感性”HLA分子形成的复合体中变化的关节蛋白,揭示类风湿性关节炎的发展可能有一个免疫标志,研究结果RA诊断开发提供了一个潜在的途径,加深了现有医学对这些HLA分子如何使个体更容易患上RA的理解。所提供的洞察力可能极大地有助于实现生产个性化药物和/或临床前干预措施来治疗类风湿性关节炎的长期目标。

原始出处:

More information: J.J. Lim el al., "The shared susceptibility epitope of HLA-DR4 binds citrullinated self-antigens and the TCR," Science Immunology (2021). immunology.sciencemag.org/look … 6/sciimmunol.abe0896

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    2021-04-23 lmm397
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    2021-04-23 jichang
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    2021-04-22 ms2000001941864021

    长知识了

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