Eur J Obstet Gynecol Reprod Biol. 2026 Sep 8;327:115435. doi: 10.1016/j.ejogrb.2026.115435. Online ahead of print.

ABSTRACT

IMPORTANCE: Endometriosis is a chronic inflammatory disease affecting approximately 10% of reproductive-age women. Immune dysregulation is central to its pathophysiology and interleukin-10 (IL-10) may contribute to immune tolerance, angiogenesis, and fibrosis.

OBJECTIVE: To review evidence on IL-10 levels in women with and without endometriosis.

SEARCH STRATEGY: PubMed, MEDLINE, and Scopus were searched from January 2015 to December 2025, following the PRISMA 2020 guidelines.

SELECTION CRITERIA: Original human studies assessing IL-10 protein levels or gene expression in women with confirmed endometriosis and controls were included. Data extraction focused on study design, population, biological sample, IL-10 assessment method, and results. Risk of bias was assessed using the JBI Critical Appraisal Tools. Meta-analysis was not performed due to methodological and reporting heterogeneity.

MAIN RESULTS: Of 441 records, 27 studies involving 5,038 women met the inclusion criteria. IL-10 was measured in serum, plasma, peritoneal fluid, follicular fluid, and endometrial tissue by ELISA or RT-qPCR. Most studies reported differences in IL-10 levels or expression between women with endometriosis and controls, although no statistically significant differences were found in some studies. Findings varied by biological compartment. Local measurements, particularly in peritoneal fluid and endometriotic tissue, more consistently demonstrated elevated IL-10. In serum, results were more heterogeneous.

CONCLUSION: IL-10 alterations are frequently reported in women with endometriosis, particularly in local biological environments. However, findings remain heterogeneous, especially for systemic measurements. Variability in study design, biological matrices, and IL-10 assessment methods underscores the need for standardised studies to clarify its pathophysiological role.

PMID:42727498 | DOI:10.1016/j.ejogrb.2026.115435