| First Author | Chinen T | Year | 2011 |
| Journal | Nat Commun | Volume | 2 |
| Pages | 190 | PubMed ID | 21304519 |
| Mgi Jnum | J:220939 | Mgi Id | MGI:5637485 |
| Doi | 10.1038/ncomms1181 | Citation | Chinen T, et al. (2011) Prostaglandin E2 and SOCS1 have a role in intestinal immune tolerance. Nat Commun 2:190 |
| abstractText | Interleukin 10 (IL-10) and regulatory T cells (Tregs) maintain tolerance to intestinal microorganisms. However, Il10(-/-)Rag2(-/-) mice, which lack IL-10 and Tregs, remain healthy, suggesting the existence of other mechanisms of tolerance. Here, we identify suppressor of cytokine signalling 1 (SOCS1) as an essential mediator of immune tolerance in the intestine. Socs1(-/-)Rag2(-/-) mice develop severe colitis, which can be prevented by the reduction of microbiota and the transfer of IL-10-sufficient Tregs. Additionally, we find an essential role for prostaglandin E2 (PGE2) in the maintenance of tolerance within the intestine in the absence of Tregs. Socs1(-/-) dendritic cells are resistant to PGE2-mediated immunosuppression because of dysregulated cytokine signalling. Thus, we propose that SOCS1 and PGE2, potentially interacting together, act as an alternative intestinal tolerance mechanism distinct from IL-10 and Tregs. |
