| First Author | Lehmann FM | Year | 2020 |
| Journal | Nat Commun | Volume | 11 |
| Issue | 1 | Pages | 1794 |
| PubMed ID | 32286285 | Mgi Jnum | J:287167 |
| Mgi Id | MGI:6405945 | Doi | 10.1038/s41467-020-15612-2 |
| Citation | Lehmann FM, et al. (2020) Microbiota-induced tissue signals regulate ILC3-mediated antigen presentation. Nat Commun 11(1):1794 |
| abstractText | Although group 3 innate lymphoid cells (ILC3s) are efficient inducers of T cell responses in the spleen, they fail to induce CD4(+) T cell proliferation in the gut. The signals regulating ILC3-T cell responses remain unknown. Here, we show that transcripts associated with MHC II antigen presentation are down-modulated in intestinal natural cytotoxicity receptor (NCR)(-) ILC3s. Further data implicate microbiota-induced IL-23 as a crucial signal for reversible silencing of MHC II in ILC3s, thereby reducing the capacity of ILC3s to present antigen to T cells in the intestinal mucosa. Moreover, IL-23-mediated MHC II suppression is dependent on mTORC1 and STAT3 phosphorylation in NCR(-) ILC3s. By contrast, splenic interferon-gamma induces MHC II expression and CD4(+) T cell stimulation by NCR(-) ILC3s. Our results thus identify biological circuits for tissue-specific regulation of ILC3-dependent T cell responses. These pathways may have implications for inducing or silencing T cell responses in human diseases. |
