Circumvention of luteolysis reveals parturition pathways in mice dependent upon innate type 2 immunity.

Autor:	Siewiera J; Department of Laboratory Medicine, University of California, San Francisco, San Francisco, CA 94143, USA., McIntyre TI; Biomedical Sciences Program, University of California, San Francisco, San Francisco, CA 94143, USA., Cautivo KM; Department of Laboratory Medicine, University of California, San Francisco, San Francisco, CA 94143, USA., Mahiddine K; Department of Laboratory Medicine, University of California, San Francisco, San Francisco, CA 94143, USA., Rideaux D; Department of Laboratory Medicine, University of California, San Francisco, San Francisco, CA 94143, USA., Molofsky AB; Department of Laboratory Medicine, University of California, San Francisco, San Francisco, CA 94143, USA; Biomedical Sciences Program, University of California, San Francisco, San Francisco, CA 94143, USA; Bakar ImmunoX Initiative, University of California, San Francisco, San Francisco, CA 94143, USA., Erlebacher A; Department of Laboratory Medicine, University of California, San Francisco, San Francisco, CA 94143, USA; Biomedical Sciences Program, University of California, San Francisco, San Francisco, CA 94143, USA; Bakar ImmunoX Initiative, University of California, San Francisco, San Francisco, CA 94143, USA; Center for Reproductive Sciences, University of California, San Francisco, San Francisco, CA 94143, USA. Electronic address: adrian.erlebacher@ucsf.edu.
Jazyk:	angličtina
Zdroj:	Immunity [Immunity] 2023 Mar 14; Vol. 56 (3), pp. 606-619.e7. Date of Electronic Publication: 2023 Feb 06.
DOI:	10.1016/j.immuni.2023.01.005
Abstrakt:	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. Competing Interests: Declaration of interests The authors declare no competing interests. (Copyright © 2023 Elsevier Inc. All rights reserved.)
Databáze:	MEDLINE
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