Pathogenesis of endometriosis: natural immunity dysfunction or autoimmune disease?

Giuseppe Matarese, De Placido G, Giuseppe De Placido, Nikas Y, Yorgos Nikas, Carlo Alviggi
Trends in molecular medicine · 2003 · vol. 9(5) , pp. 223–228 · doi:10.1016/s1471-4914(03)00051-0 · PMID:12763528 · W2031924019
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

This review explores the debate surrounding endometriosis as either a result of innate immunity dysfunction or an autoimmune condition.

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Abstract

Endometriosis is a chronic inflammatory disease, characterized by implantation and growth of endometrial tissue outside the uterine cavity. This disabling condition is considered one of the most frequent diseases in gynecology, affecting 15-20% of women in their reproductive life. Pelvic endometriosis, the most common form of the disease, is associated with increased secretion of pro-inflammatory cytokines, neo-angiogenesis, intrinsic anomalies of the refluxed endometrium and impaired function of cell-mediated natural immunity. Recently, endometriosis has also been considered to be an autoimmune disease, owing to the presence of autoantibodies, the association with other autoimmune diseases and recurrent immune-mediated abortion. These findings are in apparent contradiction with the reduced cell-mediated natural immunity observed during the disease. In this review, we focus on the multiple processes underlying the complex pathogenesis of endometriosis, with particular emphasis on the role played by the immune system with the induction of autoimmunity.

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Condition tags

endometriosis

MeSH descriptors

Autoimmune Diseases Endometriosis Animals Autoimmune Diseases Autoimmune Diseases Endometriosis Endometriosis Endometrium Endometrium Female Humans Killer Cells, Natural Killer Cells, Natural Macrophages Macrophages Peritoneum Peritoneum

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 (60)

Cited by (50)

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License: CC0 · commercial use OK