Celiac disease and transglutaminase 2: a model for posttranslational modification of antigens and HLA association in the pathogenesis of autoimmune disorders.
Celiac disease and transglutaminase 2: a model for posttranslational modification of antigens and HLA association in the pathogenesis of autoimmune disorders.
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DOI：
10.1016/j.coi.2011.08.006
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发表时间：
2011-12
影响因子：
7
通讯作者：
Jabri B
中科院分区：
文献类型：
--
作者：
Sollid LM;Jabri B
抗原的翻译后修饰（PTM）是一种打破T细胞对自身抗原耐受性并促进自身免疫的方法。然而，修饰促进自身免疫性T细胞应答的确切机制以及它们如何与特定的自身免疫相关MHC分子相关仍然难以捉摸。乳糜泻是一种具有强烈HLA关联的T细胞介导的肠病，其中免疫应答主要针对已被转氨酶2修饰的脱酰胺谷物谷蛋白肽。该疾病的特征还在于具有非常高的疾病特异性和敏感性的转氨酶2的自身抗体。乳糜泻发病机制的知识有了重要的进展，这些见解可能适用于翻译后修饰发挥作用的其他自身免疫性疾病。这一发现为理解PTM参与其他自身免疫性疾病提供了线索。
Posttranslational modification (PTM) of antigen is a way to break T-cell tolerance to self-antigens and promote autoimmunity. However, the precise mechanisms by which modifications would facilitate autoimmune T-cell responses and how they relate to particular autoimmune-associated MHC molecules remain elusive. Celiac disease is a T-cell mediated enteropathy with a strong HLA association where the immune response is directed mainly against deamidated cereal gluten peptides that have been modified by the enzyme transglutaminase 2. The disease is further characterized by autoantibodies to transglutaminase 2 that have extraordinary high disease specificity and sensitivity. There have been important advances in the knowledge of celiac disease pathogenesis, and these insights may be applicable to other autoimmune disorders where posttranslational modification plays a role. This insight gives clues for understanding the involvement of PTMs in other autoimmune diseases.
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作者：
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通讯作者：
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