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Review
, 39 (1), 9-19

The Interplay Between the Intestinal Microbiota and the Immune System

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Review

The Interplay Between the Intestinal Microbiota and the Immune System

Yuk Man Kevin Lei et al. Clin Res Hepatol Gastroenterol.

Abstract

The relationship between commensal microbes and their hosts has been studied for many years. Commensal microorganisms are known to have a significant role in regulating the physiology of their hosts and preventing pathogenic infections while the hosts' immune system is important in determining the composition of the microbiota. More recently, specific effects of the intestinal microbiota on the local and distal immune systems have been uncovered with important consequences for health and disease, and alterations in intestinal microbial composition has been associated with various disease states. Here, we will review the current understanding of the microbiota/immune system crosstalk, highlight the clinical consequences of changes in the microbiota and consider how to harness this symbiotic relationship to improve public health.

Figures

Figure 1
Figure 1. A model of the interplay between the intestinal microbiota and the mucosal immune system
Intestinal bacteria are segregated to the intestinal lumen by a physical barrier that includes goblet cells and Paneth cells which produce mucus and anti-microbial peptides (AMPs), respectively. The AMPs, secretory IgA (sIgA), mucus layer and IEC epidermal layer help control bacterial translocation and shape the microbial composition. Dendritic cells (DCs) constantly sample luminal contents to keep the mucosal immune system at its basal poised state and induce a balance of effector and regulatory cells. CX3CR1+ DCs are shown to sample luminal antigens and transfer them to CD103+ DCs that drive downstream adaptive immune responses, such as activation of T and B cells. With the help of various bacteria or microbial components and metabolic products, activated T cells differentiate into effector (Teff) and regulatory T (Treg) cells. B cells receive signals from various cell types and differentiate into IgA-secreting plasma cells, whose product, IgA, translocates across the epithelial barrier. RORγt+ ILC3s that can respond to intestinal macrophages support the function of Paneth cells, CD103+ DCs and B cells, whereas there can be a reciprocal negative regulation between ILC3s and T cells.

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