Immunology and Endometriosis

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AI-generated summary by claude@2026-06, 2026-06-08

This review details how immune alterations, including macrophage activation and reduced natural killer cell function, contribute to endometriosis development and implantation.

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Abstract

PROBLEM: Accumulating data suggests that aberrant immune responses during retrograde menstruation may be involved in the development of endometriosis. METHOD OF STUDY: The role of immunology in the etiology of endometriosis is reviewed and summarized from the available literature. RESULTS: Immunologic factors may affect a woman's susceptibility to implantation of exfoliated endometrial cells. Immune alterations include increased number and activation of peritoneal macrophages, decreased T cell reactivity and natural killer cell cytotoxicity, increased circulating antibodies, and changes in the cytokine network. CONCLUSION: There is substantial evidence that immunologic factors play a role in the pathogenesis of endometriosis and endometriosis-associated infertility. Decreased natural killer cell cytotoxicity leads to an increased likelihood of implantation of endometriotic tissue. In addition, macrophages and a complex network of locally produced cytokines modulate the growth and inflammatory behavior of ectopic endometrial implants.

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Condition tags

mesh:D004715endometriosisinfertility

MeSH descriptors

Endometriosis Menstruation Disturbances Endometriosis Endometriosis Female Humans Menstruation Disturbances Menstruation Disturbances Models, Immunological

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 (50)

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: 2026-05-13T22:12:44.121522+00:00
License: CC0 · commercial use OK