Immunopathogenesis of endometriosis: An overview of the role of innate and adaptive immune cells and their mediators

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AI-generated summary by claude@2026-06, 2026-06-07

This review examines how innate and adaptive immune cells and their mediators contribute to the inflammatory and later immunosuppressive environment that promotes endometriosis progression.

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Abstract

Abstract Background Endometriosis is a chronic inflammatory disease associated with the growth and proliferation of endometrial‐like tissues outside the uterus. Although the exact etiology and mechanism of the pathogenesis of the disease have not been fully elucidated, the immune system cells and the mediators produced by them can be named as effective factors in the onset and progression of the disease. Aims We aim to attempt to review studies on the role of the immune system in endometriosis to better understand the pathogenesis of endometriosis. Content Abundant production of inflammatory mediators by neutrophils and macrophages and reduced cytotoxicity of defined cells promote endometriosis at the early stages of the disease. Following an increase in the inflammation of the environment, the body takes compensatory mechanisms to reduce inflammation and establish homeostasis. For this purpose, the body produces remodeling and anti‐inflammatory factors leading to slow conversion of the inflammatory environment into a non‐inflammatory environment with proliferative and immunosuppressive properties. Environmental conditions induce M2 macrophages, TH2 cells, and Tregs differentiation, promoting disease progression by producing angiogenic and immunosuppressive factors. However, the exact molecular mechanism involved in changing inflammatory to non‐inflammatory conditions is not yet fully understood. Implications Due to the common characteristics of endometriotic cells and cancer cells, most potential treatment options for endometriosis have been suggested due to the results of these methods in the treatment of cancer. In this pathway, immune system cells and soluble mediators can be used as targets.

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Condition tags

mesh:D004715endometriosis

MeSH descriptors

Endometriosis Endometrium Endometrium Female Humans Inflammation Macrophages Macrophages Neutrophils Neutrophils

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (100)

Cited by (26)

Source provenance

europepmc
last seen: 2026-06-04T01:30:01.192114+00:00
openalex
last seen: 2026-06-04T00:00:01.174412+00:00
pubmed
last seen: 2026-05-13T22:23:57.700195+00:00
License: CC0 · commercial use OK