| Theme | Impacts of intestinal microbiota | |
|---|---|---|
| Title | Gut microbiota and intestinal immunity | |
| Publish Date | 2017/07 | |
| Author | Hiroshi Ohno | Laboratory for Intestinal Ecosystem, RIKEN Center for Integrative Medical Sciences (IMS) |
| [ Summary ] | Animal guts harbor great numbers of commensal bacteria. Our gut does not unconditionally accept the gut microbiota. Rather it tries to contain them by secreting IgA. To this end, there exist M cells, a subset of epithelial cells specialized for bacterial uptake, in the region of epithelium termed the follicleassociated epithelium (FAE), which covers the lymphoid follicles of gut-associated lymphoid tissue (GALT) such as Payer's patches (PPs). M cells express bacterial uptake receptors, such as GP2 and cellular prion protein, on their luminal surfaces to transfer taken up bacteria to GALT for initiation of intestinal immune responses. A transcription factor, Spi-B, is essential for M-cell differentiation. A subset of PP dendritic cells express IL-22BP, which captures IL-22 to block IL-22 signaling in FAE and confers on FAE its characteristic of suppressed production of mucus and anti-microbial peptides for better access to bacteria. Gut microbiota also modulate differentiation of various Th subsets. Those Th cells which are dependent on diversification of the IgA repertoire are reciprocally required for maintenance of normal gut microbiota diversity. Gut microbiota-dictated Th17 and Treg differentiations are also important for intestinal immune homeostasis. |
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