Epigenetic regulation and T-cell responses in endometriosis – something other than autoimmunity

Dariusz Szukiewicz
Frontiers in immunology · 2022 · vol. 13 , pp. 943839 · doi:10.3389/fimmu.2022.943839 · PMID:35935991 · PMC9355085 · W4286560196
review OA: gold CC0 ⤵ 34 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

This review explores epigenetic reprogramming of T cells, including DNA methylation and histone modifications, as a key factor in endometriosis pathophysiology and suggests potential epigenetic modulation-based therapies.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 ⓘ

This paper is a state-of-the-art review describing how epigenetic mechanisms that regulate T-cell responses (including DNA methylation and histone modifications) may contribute to endometriosis pathophysiology, in the broader context of immune dysregulation and the documented coexistence of endometriosis with autoimmune phenomena. It summarizes evidence of altered Treg populations and shifts in Th1/Th2 balance reported in endometriosis-associated peritoneal fluid and endometrial tissues, and explains how heritable, non–DNA-sequence changes could shape immune transcriptional programs and tissue inflammation. A key limitation is that the article is largely a narrative review aiming to outline the “state of the art” rather than presenting new experimental data, and it reiterates that the etiology of endometriosis remains unknown. This paper is centrally about endometriosis — it focuses on epigenetic reprogramming of T cells as a proposed factor in endometriosis-related immune dysfunction.

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Abstract

Endometriosis is defined as the presence of endometrial-like glands and stroma located outside the uterine cavity. This common, estrogen dependent, inflammatory condition affects up to 15% of reproductive-aged women and is a well-recognized cause of chronic pelvic pain and infertility. Despite the still unknown etiology of endometriosis, much evidence suggests the participation of epigenetic mechanisms in the disease etiopathogenesis. The main rationale is based on the fact that heritable phenotype changes that do not involve alterations in the DNA sequence are common triggers for hormonal, immunological, and inflammatory disorders, which play a key role in the formation of endometriotic foci. Epigenetic mechanisms regulating T-cell responses, including DNA methylation and posttranslational histone modifications, deserve attention because tissue-resident T lymphocytes work in concert with organ structural cells to generate appropriate immune responses and are functionally shaped by organ-specific environmental conditions. Thus, a failure to precisely regulate immune cell transcription may result in compromised immunological integrity of the organ with an increased risk of inflammatory disorders. The coexistence of endometriosis and autoimmunity is a well-known occurrence. Recent research results indicate regulatory T-cell (Treg) alterations in endometriosis, and an increased number of highly active Tregs and macrophages have been found in peritoneal fluid from women with endometriosis. Elimination of the regulatory function of T cells and an imbalance between T helper cells of the Th1 and Th2 types have been reported in the endometria of women with endometriosis-associated infertility. This review aims to present the state of the art in recognition epigenetic reprogramming of T cells as the key factor in the pathophysiology of endometriosis in the context of T-cell-related autoimmunity. The new potential therapeutic approaches based on epigenetic modulation and/or adoptive transfer of T cells will also be outlined.

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Condition tags

endometriosischronic_pelvic_paininfertility

MeSH descriptors

Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Infertility Infertility Infertility Infertility Infertility Autoimmunity Autoimmunity Autoimmunity Autoimmunity Endometrium Endometrium Endometrium Endometrium Epigenesis, Genetic Epigenesis, Genetic

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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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