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Recent Advances on Microbiota Involvement in the Pathogenesis of Autoimmunity

机译:Microbiota参与自身免疫发病机制的最新进展

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摘要

Autoimmune disorders derive from genetic, stochastic, and environmental factors that all together interact in genetically predisposed individuals. The impact of an imbalanced gut microbiome in the pathogenesis of autoimmunity has been suggested by an increasing amount of experimental evidence, both in animal models and humans. Several physiological mechanisms, including the establishment of immune homeostasis, are influenced by commensal microbiota in the gut. An altered microbiota composition produces effects in the gut immune system, including defective tolerance to food antigens, intestinal inflammation, and enhanced gut permeability. In particular, early findings reported differences in the intestinal microbiome of subjects affected by several autoimmune conditions, including prediabetes or overt disease compared to healthy individuals. The present review focuses on microbiota-host homeostasis, its alterations, factors that influence its composition, and putative involvement in the development of autoimmune disorders. In the light of the existing literature, future studies are necessary to clarify the role played by microbiota modifications in the processes that cause enhanced gut permeability and molecular mechanisms responsible for autoimmunity onset.
机译:自身免疫性疾病来自遗传,随机和环境因素,所有这些因素都在一起在遗传倾向的个体中相互作用。通过越来越多的实验证据,在动物模型和人类中,已经提出了在自身免疫发病机制中的影响。包括建立免疫稳态的一些生理机制受到肠道中的共生微生物群的影响。改变的微生物群组合物在肠道免疫系统中产生效果,包括对食物抗原,肠炎症和增强的肠道渗透性有缺陷的耐受性。特别是,早期发现报告了受几种自身免疫条件影响的受试者的肠道微生物的差异,包括与健康个体相比的前脂肪酸或明显疾病。本综述重点介绍了微生物亚宿主宿主,其改变,影响其构成的因素,以及推定参与自身免疫性障碍的发展。根据现有文献,未来的研究是必要的,以澄清在引起肠道渗透率和负责自身免疫发作的肠道渗透率和分子机制的过程中的方法所发挥的作用。

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