| First Author | Siewiera J | Year | 2023 |
| Journal | Immunity | Volume | 56 |
| Issue | 3 | Pages | 606-619.e7 |
| PubMed ID | 36750100 | Mgi Jnum | J:347463 |
| Mgi Id | MGI:7448326 | Doi | 10.1016/j.immuni.2023.01.005 |
| Citation | Siewiera J, et al. (2023) Circumvention of luteolysis reveals parturition pathways in mice dependent upon innate type 2 immunity. Immunity 56(3):606-619.e7 |
| abstractText | Although mice normally enter labor when their ovaries stop producing progesterone (luteolysis), parturition can also be triggered in this species through uterus-intrinsic pathways potentially analogous to the ones that trigger parturition in humans. Such pathways, however, remain largely undefined in both species. Here, we report that mice deficient in innate type 2 immunity experienced profound parturition delays when manipulated endocrinologically to circumvent luteolysis, thus obliging them to enter labor through uterus-intrinsic pathways. We found that these pathways were in part driven by the alarmin IL-33 produced by uterine interstitial fibroblasts. We also implicated important roles for uterine group 2 innate lymphoid cells, which demonstrated IL-33-dependent activation prior to labor onset, and eosinophils, which displayed evidence of elevated turnover in the prepartum uterus. These findings reveal a role for innate type 2 immunity in controlling the timing of labor onset through a cascade potentially relevant to human parturition. |
