ArticleJCI insight2021
IL-33 activates group 2 innate lymphoid cell expansion and modulates endometriosis.
Article in JCI insight, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.
- The role of fibrosis in endometriosis: a systematic review.Human reproduction update · 2024Pooled it
- Cancer-associated mutations in endometriosis reframe a benign disease through molecular oncology.Molecular oncology · 2026Review
- Flowing differently: exploratory characterization of menstrual effluent compared with peripheral blood.F&S science · 2026Article
- Contributions of T-helper 9 cells in endometriosis-associated inflammation and lesion growth.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Endometriosis immune microenvironment timing shifts: from immune escape to immune exhaustion.Cell death discovery · 2026Review
- The role of IL-33/ST2 signaling in female reproductive diseases.Frontiers in cell and developmental biology · 2026Review
- Dysregulation of Key Biological Processes in Endometriosis Pathophysiology.Current molecular medicine · 2026Review
- Tissue-Resident ILC2s Across Organs: Heterogeneity, Niche Crosstalk, and Shared Regulatory Circuits.Immune network · 2025Review
- Pro-endometriosis macrophage release of IL-33 is key for endometriosis pain and lesion formation.bioRxiv : the preprint server for biology · 2025Article
- The Immune Microenvironment: New Therapeutic Implications in Organ Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Macrophage Plasticity and Extracellular Vesicles in Endometriosis: Immunopathology and Therapeutic Perspectives.Reproductive sciences (Thousand Oaks, Calif.) · 2025Review
- Innate Lymphoid Cells in Reproductive Health and Disease.European journal of immunology · 2025Review
- Regulatory network analysis of Dclk1 gene expression reveals a tuft cell-ILC2 axis that inhibits pancreatic tumor progression.Cell reports · 2025Article
- Endometriosis: An Immunologist's Perspective.International journal of molecular sciences · 2025Review
- Biological mechanisms and therapeutic prospects of interleukin-33 in pathogenesis and treatment of allergic disease.Journal of inflammation (London, England) · 2025Review
- Infertility, IL-17, IL-33 and Microbiome Cross-Talk: The Extended ARIA-MeDALL Hypothesis.International journal of molecular sciences · 2024Review
- Regulatory network analysis ofbioRxiv : the preprint server for biology · 2024Article
- The IL-33-ST2 axis plays a vital role in endometriosis via promoting epithelial-mesenchymal transition by phosphorylating β-catenin.Cell communication and signaling : CCS · 2024Article
- IL-33 and soluble ST2 in follicular fluid are associated with premature ovarian insufficiency.Frontiers in endocrinology · 2024Article
- Causal Relationship Between Endometriosis and Pelvic Inflammatory Diseases: Mendelian Randomization Study.International journal of women's health · 2024Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Chronic inflammation and localized alterations in immune cell function are suspected to contribute to the progression of endometriosis and its associated symptoms. In particular, the alarmin IL-33 is elevated in the plasma, peritoneal fluid, and endometriotic lesions from patients with endometriosis; however, the exact role of IL-33 in the pathophysiology of endometriosis is not well understood. In this study, we demonstrate, in both humans and a murine model, that IL-33 contributes to the expansion of group 2 innate lymphoid cells (ILC2s), and this IL-33-induced ILC2 expansion modulates the endometriosis lesion microenvironment. Importantly, we show that IL-33 drives hallmarks of severe endometriosis, including elevated inflammation, lesion proliferation, and fibrosis, and that this IL-33-induced aggravation is mediated by ILC2s. Finally, we demonstrate the functionality of IL-33 neutralization as a promising and potentially novel therapeutic avenue for treating the debilitating symptoms of endometriosis.
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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 OpenQuestion graph.