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肠道共生菌、菌群失调和免疫反应失衡在多发性硬化症发病机制中的作用。

Gut commensals, dysbiosis, and immune response imbalance in the pathogenesis of multiple sclerosis.

机构信息

Paul L. Foster School of Medicine, Texas Tech University Health Sciences Center El Paso, El Paso, TX, USA.

The Jackson Laboratory for Genomic Medicine, Farmington, CT, USA.

出版信息

Mult Scler. 2021 May;27(6):807-811. doi: 10.1177/1352458520928301. Epub 2020 Jun 8.

DOI:10.1177/1352458520928301
PMID:32507072
Abstract

Intestinal microbiota alterations have been found to be directly related to a wide range of disease states in humans, including multiple sclerosis (MS). The etiology of MS is highly debated and subsequently, there is no cure. Research dedicated to MS and its murine model, experimental autoimmune encephalomyelitis (EAE), have found that dysbiosis of the gut microbiota may play a role in the disease state and severity. In this review, we discuss the characteristic dysbiosis in MS, the role commensal-derived ligands may have in the pathogenesis of the disease, and the possibility of targeting the microbiota as a future therapy.

摘要

肠道微生物群的改变已被发现与人类的多种疾病状态直接相关,包括多发性硬化症(MS)。MS 的病因仍存在争议,因此目前尚无治愈方法。针对 MS 及其小鼠模型实验性自身免疫性脑脊髓炎(EAE)的研究发现,肠道微生物群的失调可能在疾病状态和严重程度中发挥作用。在这篇综述中,我们讨论了 MS 的特征性菌群失调、共生衍生配体在疾病发病机制中的可能作用,以及将微生物组作为未来治疗靶点的可能性。

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