Prostaglandin E2 and SOCS1 have a role in intestinal immune tolerance.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 21304519.
- Also identified by DOI 10.1038/ncomms1181 and PMC identifier 3105338.
- Licence recorded as CC BY-NC-SA.
- Because redistribution is not established, this page shows the abstract only. Follow the links below for the full text.
Abstract
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.
Medical subject headings
- Dinoprostone
- Immune Tolerance
- Intestines
- Suppressor of Cytokine Signaling Proteins