乳糜泻:遗传和免疫的作用以及新治疗策略的最新进展

E. Sequeira, Ginpreet Kaur, H. Buttar
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引用次数: 1

摘要

乳糜泻(CD)是最常见的小肠炎症性疾病之一,可导致人类腹痛、腹泻、吸收不良、体重减轻、厌食和缺铁性贫血。它是一种人类白细胞抗原(HLA)相关的疾病,由小麦和相关谷物中的麸质和麦胶蛋白引发。其他遗传因素如HLA-DQ2和HLA-DQ8的存在也被确定为产生循环自身抗体转谷氨酰胺酶(TG2)。TG2酶使谷蛋白肽脱酰胺并增加其对HLA-DQ2或HLA-DQ8的亲和力,进而引起CD4+ t -辅助性1 (Th1)细胞更强烈的激活并触发免疫反应,这种免疫级联最终导致肠膜损伤和吸收不良。一般来说,乳糜泻需要终生无谷蛋白饮食。然而,严格遵守无麸质饮食是困难的,并不总是有效的。一些治疗乳糜泻的药物和替代疗法目前正在开发和临床试验中,本综述的目的是强调遗传和免疫在乳糜泻中的复杂参与,并重点介绍用于开发治疗乳糜泻的辅助和替代疗法的新策略。25: 45-58。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Celiac disease: Role of genetics and immunity and update on novel strategies for treatment
Celiac disease (CD) is one of the most common inflammatory diseases of the small intestine which causes abdominal pain, diarrhoea, malabsorption, weight loss, anorexia, and iron deficiency anaemia in humans. It is a human leukocyte antigen (HLA)-linked disorder that is triggered by the gluten and gliadin proteins from wheat and related cereals. The presence of other genetic factors such as HLA-DQ2 and HLA-DQ8 have also been identified for the generation of circulating autoantibodies to the enzyme transglutaminase (TG2). The TG2 enzyme deamidates the gluten peptides and increases their affinity for the HLA-DQ2 or HLA-DQ8, which in turn cause a more vigorous activation of CD4+ T-helper 1 (Th1) cells and trigger the immune response, and such immune cascade eventually leads to intestinal membrane damage and malabsorption. Generally, CD is managed by lifelong gluten-free diet. However, strict adherence to a gluten-free diet is difficult and is not always effective. Several pharmacological agents and alternative therapies for treating CD are currently under development and are in clinical trials, The purpose of this review is to highlight the complex involvement of genetics and immunity in CD and to focus on the novel strategies being used for developing adjunct and alternative therapies for the treatment of CD. Biomedical Reviews 2014; 25: 45-58.
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