ArticleImmunity2023
Circumvention of luteolysis reveals parturition pathways in mice dependent upon innate type 2 immunity.
Article in Immunity, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
9 citing papers in PubMed, 0 citations in OpenAlex.
- Interleukin-33 and its receptor: multifaceted roles and emerging therapeutic potential.Nature reviews. Immunology · 2026Review
- The postpartum uterus reveals compartment-specific remodeling processes with distinct immune signatures.Frontiers in immunology · 2026Article
- Tissue-Resident ILC2s Across Organs: Heterogeneity, Niche Crosstalk, and Shared Regulatory Circuits.Immune network · 2025Review
- Immune system influence on physiology.Science (New York, N.Y.) · 2025Review
- Innate Lymphoid Cells in Reproductive Health and Disease.European journal of immunology · 2025Review
- Article
- The hormonal control of parturition.Physiological reviews · 2024Review
- Sexual dimorphism in skin immunity is mediated by an androgen-ILC2-dendritic cell axis.Science (New York, N.Y.) · 2024Article
- Human embryo implantation.Development (Cambridge, England) · 2023Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.