The role of selected populations of immune cells in the pathogenesis of endometriosis

Dorota Suszczyk, Anna Pawłowska, Karolina Okła, Klaudia Parafiniuk, Grzegorz Polak, Jan Kotarski, Iwona Wertel
In: Current Gynecologic Oncology · 2018 · vol. 16(3) , pp. 167–176 · doi:10.15557/cgo.2018.0020 · W2914284357
article OA: bronze CC0 ⤵ 3 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-23 ⓘ

This paper investigated the role of specific immune cell populations in the development of endometriosis, a condition where endometrial tissue grows outside the uterus, leading to tissue invasion and organ dysfunction.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-23 · read from full text ⓘ

The paper reviews endometriosis by examining how disturbances in immune-cell number and function—covering peripheral and peritoneal macrophages, NK cells, cytotoxic lymphocytes, dendritic cells, regulatory T cells, and myeloid-derived suppressor cells—affect processes such as survival, implantation, proliferation, and angiogenesis of ectopic endometrial tissue. It synthesizes evidence that altered activity of these cells may impair elimination of menstrual blood and apoptotic cells, contributing to the persistence of endometrial foci. A key limitation is that it remains unclear whether immune dysfunction is a cause of endometriosis or instead a consequence of ectopic endometrial proliferation. This paper is centrally about endometriosis — it focuses on the role of selected immune cell populations in the condition’s pathogenesis.

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Abstract

Endometrioza diagnozowana jest u okoo 5-10% kobiet w wieku rozrodczym i charakteryzuje si wystpowaniem tkanki endometrium poza jam macicy. Przemieszczone komrki endometrium maj zdolno naciekania okolicznych tkanek i odlegych narzdw, co prowadzi do ich dysfunkcji
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The role of selected populations of immune cells in the pathogenesis of endometriosis Endometriosis is diagnosed in approximately 5–10% of women in their childbearing years and is characterized by the presence of endometrial tissue outside the uterus. The translocated endometrial cells are able to infiltrate adjacent tissues and distant organs, leading to their dysfunction. Despite numerous studies on the pathogenesis of endometriosis, its etiology has not yet been clearly explained. Predisposing factors include hyperestrogenism, congenital uterine anomalies, early menarche, and short menstrual cycles with long and heavy bleeding. Disturbances in the number and function of immune cells as well as the presence of factors determining the survival, implantation and proliferation of endometrial cells have been shown in patients with endometriosis. The activity of both peripheral and peritoneal macrophages, NK cells, cytotoxic lymphocytes and dendritic cells is affected. These cells are responsible for eliminating erythrocytes, menstrual blood cells and cells undergoing apoptosis. Furthermore, the latest research indicates the presence and altered activity of regulatory T cells and myeloid-derived suppressor cells in patients with endometriosis. However, it is still not known whether dysfunctions of these cell populations induce endometriosis or whether they are a consequence of ectopic endometrial proliferation. According to latest reports, endometrial foci may be precursors of endometrioid or clear-cell ovarian carcinoma. A thorough understanding of the mechanisms underlying the disorders associated with the above-mentioned cell populations may be crucial for identifying patients at increased risk of endometriosis-associated ovarian tumor and implementing appropriate preventive measures. The paper describes the role of selected immune cell populations in stimulating implantation, proliferation and angiogenesis in patients with endometriosis.

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endometriosis

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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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