The role of the immune response in the etiopathogenesis of endometriosis

Cătălina Diana Stănică, Neacsu Adrian, Romina‐Marina Sima, Raluca Gabriela Ioan
In: Romanian Medical Journal · 2021 · vol. 68(1) , pp. 40–47 · doi:10.37897/rmj.2021.1.7 · W3176215564
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

This review explores how altered immune responses, including cellular and humoral immunity and autoantibodies, contribute to the development and progression of endometriosis.

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Abstract

Endometriosis is a benign, chronic, estrogen-dependent condition, present in 10% of women of reproductive age. The condition is associated with chronic pelvic pain and infertility that influence their quality of life, as well as married life and has important socio-economic consequences. Despite its high morbidity, its etiopathogenesis is incompletely known. A large number of studies suggest that the ability of endometrial implants to grow in ectopic locations may be correlated with the altered immune response towards the endometriotic tissue. There are enough data to show that immune system mediators, such as cytokines and chemokines, are playing key roles in the onset and olso on progression of endometriosis. There are studies that prove the association between endometriosis and autoimmune diseases. The present paper aims to investigate the implications of the immune response in the etiopathogenesis of endometriosis. The study of cellular or humoral immunity deficits, the presence of autoantibodies associated with this condition, can facilitate the understanding of the mechanisms that lead to the appearance and spread of endometriosis. We hope that this information will ultimately provide the basis for the development of new effective approaches in endometriosis management.

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Condition tags

endometriosischronic_pelvic_paininfertility

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.

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