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乳糜泻:朝着诊断和发病机制定义的方向取得进展。

Celiac disease: progress towards diagnosis and definition of pathogenic mechanisms.

出版信息

Int Rev Immunol. 2011 Aug;30(4):183-4. doi: 10.3109/08830185.2011.604565.

DOI:10.3109/08830185.2011.604565
PMID:21787223
Abstract

The current issue of the International Reviews of Immunology is dedicated entirely to Celiac Disease (CD). Recent development of additional biomarkers and diagnostics resulted in a sharp revision of the prevalence of this condition, with a previously unrecognized subclinical occurrence in the adult population. This was paralleled by groundbreaking progress in understanding its molecular pathogenesis: while gluten-derived peptides activate the innate immunity, post-translationally modified gluten elicits an adaptive immunity. These arms amplify each other, resulting in a self- perpetuating autoimmune condition, influenced by disturbances of the gut flora and mucus chemistry. The process evolves dramatically in a subset of patients with vulnerable immune homeostasis (eg. Treg cells) explaining the progressive, aggravating syndrome in the clinically overt version of CD. In depth understanding of the pathogenesis of CD thus creates the premises of developing novel, more accurate animal models that should support a rationale development of new prophylactic and therapeutic interventions.

摘要

本期《国际免疫学评论》专刊全部聚焦于乳糜泻(CD)。随着更多生物标志物和诊断方法的出现,该疾病的流行率出现了大幅修订,成年人中此前未被识别的亚临床病例也大量出现。与此同时,人们对其分子发病机制的理解也取得了突破性进展:虽然源于谷蛋白的肽激活了固有免疫,但经翻译后修饰的谷蛋白则引发了适应性免疫。这两个分支相互增强,导致了一种自我持续的自身免疫性疾病,这种疾病受肠道菌群和黏液化学的干扰影响。在具有脆弱免疫稳态的患者亚群中,这一过程会出现戏剧性的演变(例如 Treg 细胞),从而解释了 CD 临床显性版本中进行性加重的综合征。因此,对 CD 发病机制的深入了解为开发新型、更准确的动物模型奠定了基础,这将有助于合理开发新的预防和治疗干预措施。

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