| First Author | Polese B | Year | 2021 |
| Journal | Cell Rep | Volume | 36 |
| Issue | 4 | Pages | 109456 |
| PubMed ID | 34320346 | Mgi Jnum | J:324789 |
| Mgi Id | MGI:6876913 | Doi | 10.1016/j.celrep.2021.109456 |
| Citation | Polese B, et al. (2021) Prostaglandin E2 amplifies IL-17 production by gammadelta T cells during barrier inflammation. Cell Rep 36(4):109456 |
| abstractText | Interleukin-17 (IL-17)-producing gammadelta (gammadelta17) T cells are innate-like lymphocytes that contribute to protective anti-microbial responses but are also implicated in pathogenic inflammation at barrier sites. Understanding tissue-specific signals that regulate this subset is important to boost host defense mechanisms, but also to mitigate immunopathology. Here, we demonstrate that prostaglandin E2 (PGE2), a cyclooxygenase-dependent member of the eicosanoid family, directly enhances cytokine production by circulating and tissue-specific gammadelta17 T cells in vitro. Gain- and loss-of-function in vivo approaches further reveal that although provision of PGE2 amplifies psoriasiform inflammation, ablation of host mPGES1-dependent PGE2 synthesis is dispensable for cutaneous gammadelta17 T cell activation. By contrast, loss of endogenous PGE2 production or depletion of the gut microbiota compromises intestinal gammadelta17 T cell responses and increases disease severity during experimental colitis. Together, our results demonstrate how a lipid mediator can synergize with tissue-specific signals to enhance innate lymphocyte production of IL-17 during barrier inflammation. |
