ArticleFrontiers in immunology2020
IL-17A Modulates Peritoneal Macrophage Recruitment and M2 Polarization in Endometriosis.
Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.
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Who cites it
84 citing papers in PubMed, 120 citations in OpenAlex.
- Inflammatory Changes after Medical Suppression of Suspected Endometriosis for Implantation Failure: Preliminary Results.International journal of molecular sciences · 2024Trial
- Elevated interleukin-33, CD1c+ dendritic cells, and interleukin-17A in peritoneal fluid of patients with endometriosis: a case-control study.Molecular biology reports · 2026Article
- Do Oxidative Stress-Modified Exosomes Contribute to Infertility in Endometriosis?International journal of molecular sciences · 2026Review
- Targeting the IL-17C-M2 macrophage axis ameliorates fibrosis in endometriosis through MAPK/ERK signaling.Journal of translational medicine · 2026Article
- Article
- Targeting the Immune Network in Endometriosis: A Comprehensive Review of Pathogenesis, Immunomodulation, and Emerging Therapies.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Immune escape in endometriosis: mechanisms, reprogramming strategies, and precision interventions.Reproductive biology and endocrinology : RB&E · 2026Review
- The interaction between inflammation and estrogen in adenomyosis : from molecular mechanisms to therapeutic strategies.Seminars in immunopathology · 2026Review
- Parabacteroides goldsteinii and its metabolite 7-KLCA attenuate endometriosis via TGR5 to reprogram macrophages by modulating the PPARγ/GPR132 axis.NPJ biofilms and microbiomes · 2026Article
- Mechanisms of IL-17A Neutralisation in Alleviating Renal Fibrosis and Inflammation in Spontaneously Hypertensive Rats.Clinical and experimental pharmacology & physiology · 2026Article
- Endometriosis immune microenvironment timing shifts: from immune escape to immune exhaustion.Cell death discovery · 2026Review
- TMT1A inhibits lung adenocarcinoma progression by suppressing M2 macrophage polarization.iScience · 2026Article
- Immune dysregulation in endometriosis: the T cell perspective.Frontiers in immunology · 2026Review
- Dysregulation of Key Biological Processes in Endometriosis Pathophysiology.Current molecular medicine · 2026Review
- Metabolic-epigenetic imprinting of macrophages in endometriosis: a working model for lesion persistence and treatment.Frontiers in immunology · 2026Review
- Phlorotannins fromMarine drugs · 2025Article
- Bidirectional causal relationship between inflammatory cytokines and endometriosis at different sites.BMC women's health · 2025Article
- Identification and Validation of Novel Combinatorial Genetic Risk Factors for Endometriosis across Multiple UK and US Patient Cohorts.medRxiv : the preprint server for health sciences · 2025Article
- Endometriosis and Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: A Systematic Review and Meta-Analysis.Diagnostics (Basel, Switzerland) · 2025Review
- Streptococcus gallolyticus supernatant induces M2 macrophage polarization and activates IL-17 F signaling in colorectal tumorigenesis.Gut pathogens · 2025Article
24 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Endometriosis is a debilitating gynecological disease characterized by the extrauterine presence of endometrial-like tissues located on the peritoneal membrane and organs of the pelvic cavity. Notably, dysfunctional immune activation in women with endometriosis could also contribute to the development of disease. In particular, alternatively activated (M2) peritoneal macrophages are shown to aid peritoneal lesion development by promoting remodeling of extracellular matrix and neovascularization of lesions. However, the stimuli responsible for polarizing M2 macrophages in endometriosis remain elusive. Interleukin-17A (IL-17A) can induce M2 macrophage polarization in other disease models and IL-17A is elevated in the plasma and endometriotic lesions of women with endometriosis. In this study, we investigated whether IL-17A could induce macrophage recruitment and M2 polarization, while promoting endometriotic lesion growth through enhanced vascularization. By utilizing a co-culture of macrophage-like THP-1 cells with an endometriotic epithelial cell line, our
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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.