Microbiota-Immune Interactions Regulate Metabolic Disease.

Microbiota-Immune Interactions Regulate Metabolic Disease.
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DOI:
10.4049/jimmunol.2100419
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发表时间:
2021-10-01
影响因子:
4.4
通讯作者:
Round, June L.
Round, June L.
中科院分区:
医学2区
文献类型:
--
作者:
Klag, Kendra A.;Round, June L.

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代谢性疾病在世界范围内很常见,包括营养过剩的疾病,如肥胖症,或营养不足的疾病,如恶性营养不良症。免疫系统和微生物群都有助于各种代谢疾病;然而,在这种情况下,这两个过程在很大程度上是相互独立的。胃肠道系统容纳了最大密度的微生物,但也容纳了最大的免疫分子集合之一,特别是Abs。伊加同种型在粘膜部位的Ab景观中占主导地位,并且许多研究已经证明了这种Ab对微生物群稳定性的重要性。在这篇文章中,我们回顾了文献,展示了稳态抗体反应如何控制微生物群的组成和功能,以影响代谢疾病。我们认为,许多代谢性疾病可能是由于肠道免疫系统的稳态免疫控制受到破坏而引起的,进一步了解这种相互作用可以为治疗干预提供新的机会。
Metabolic diseases are common worldwide and include diseases of overnutrition, such as obesity, or undernutrition, such as kwashiorkor. Both the immune system and the microbiota contribute to a variety of metabolic diseases; however, these two processes have largely been studied independently of one another in this context. The gastrointestinal system houses the greatest density of microbes but also houses one of the largest collections of immune molecules, especially Abs. The IgA isotype dominates the Ab landscape at mucosal sites, and a number of studies have demonstrated the importance of this Ab to the stability of the microbiota. In this article, we review the literature that demonstrates how homeostatic Ab responses control microbiota composition and function to influence metabolic disease. We propose that many metabolic diseases may arise from disruptions to homeostatic immune control of gut commensals and that further understanding this interaction can offer a novel opportunity for therapeutic interventions.
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