Correlation Engine 2.0
Clear Search sequence regions

  • eosinophils (1)
  • female (1)
  • fibroblasts (1)
  • humans (2)
  • IL 33 (2)
  • Interleukin 33 (2)
  • labor (2)
  • labor onset (2)
  • luteolysis (4)
  • lymphocytes (2)
  • mice (4)
  • myometrium (1)
  • ovaries (1)
  • pregnancy (1)
  • progesterone (1)
  • uterus (3)
  • Sizes of these terms reflect their relevance to your search.

    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. Copyright © 2023 Elsevier Inc. All rights reserved.


    Johan Siewiera, Tara I McIntyre, Kelly M Cautivo, Karim Mahiddine, Damon Rideaux, Ari B Molofsky, Adrian Erlebacher. Circumvention of luteolysis reveals parturition pathways in mice dependent upon innate type 2 immunity. Immunity. 2023 Mar 14;56(3):606-619.e7

    Expand section icon Mesh Tags

    Expand section icon Substances

    PMID: 36750100

    View Full Text