期刊
CELL REPORTS
卷 21, 期 5, 页码 1215-1226出版社
CELL PRESS
DOI: 10.1016/j.celrep.2017.10.022
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资金
- KAKENHI from the Japanese Ministry of Education, Culture, Sports, Science and Technology [16K09374]
- Keio University Medical Fund
- Grants-in-Aid for Scientific Research [16K09374, 15K09021] Funding Source: KAKEN
Gut-derived microbial antigens trigger the innate immune system during acute liver injury. During recovery, regulatory immunity plays a role in suppressing inflammation; however, the precise mechanism underlying this process remains obscure. Here, we find that recruitment of immune-regulatory classical dendritic cells (cDCs) is crucial for liver tolerance in concanavalin A-induced acute liver injury. Acute liver injury resulted in enrichment of commensal Lactobacillus in the gut. Notably, Lactobacillus activated IL-22 production by gut innate lymphoid cells and raised systemic IL-22 levels. Gut-derived IL-22 enhanced mucosal barrier function and promoted the recruitment of regulatory cDCs to the liver. These cDCs produced IL-10 and TGF-beta through TLR9 activation, preventing further liver inflammation. Collectively, our results indicate that beneficial gut microbes influence tolerogenic immune responses in the liver. Therefore, modulation of the gut microbiota might be a potential option to regulate liver tolerance.
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