Peritoneal immune microenvironment of endometriosis: Role and therapeutic perspectives

Siman Chen, Yukai Liu, Zhiqi Zhong, Chunyan Wei, Yuyin Liu, Xiaoyong Zhu, Xiao‐Yong Zhu
Frontiers in immunology · 2023 · vol. 14 , pp. 1134663 · doi:10.3389/fimmu.2023.1134663 · PMID:36865552 · PMC9971222 · W4320724174
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

This review explores how the peritoneal immune microenvironment, involving various immune cells and cytokines, contributes to endometriosis pathogenesis and discusses potential immune-regulating diagnostic biomarkers and therapies.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-09 ⓘ

This review examines the peritoneal immune microenvironment in endometriosis, synthesizing evidence that innate and adaptive immune dysregulation after retrograde menstruation contributes to the implantation, vascularization, and fibrogenesis of ectopic endometrial lesions. It summarizes findings that peritoneal macrophages, NK cells, dendritic cells, neutrophils, T cells, and B cells—along with cytokines such as IL-1β, IL-6, IL-8, TNF-α, and TGF-β—shape a pro-inflammatory early environment that can shift toward immune tolerance, and discusses proposed mechanisms including reduced macrophage phagocytic ability, monocyte recruitment, and macrophage M1/M2 polarization (with noted conflicting views). The paper describes endocrine influences (estrogen overexpression and progesterone resistance) on immune function and outlines prospects for nonhormonal, immune microenvironment–targeted approaches and potential diagnostic biomarkers, while explicitly relying on the limitations of current hormonal therapy rather than providing new experimental data. This paper is centrally about endometriosis — it focuses on the role of the peritoneal immune microenvironment in endometriosis pathogenesis and therapeutic prospects.

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Abstract

Endometriosis, an estrogen-dependent chronic inflammatory disease characterized by the growth of endometrium-like tissues outside the uterine cavity, affects 10% of reproductive-age women. Although the pathogenesis of endometriosis is uncertain, it is widely accepted that retrograde menstruation results in ectopic endometrial tissue implantation. Given that not all women with retrograde menstruation develop endometriosis, immune factors have been hypothesized to affect the pathogenesis of endometriosis. In this review, we demonstrate that the peritoneal immune microenvironment, including innate immunity and adaptive immunity, plays a central role in the pathogenesis of endometriosis. Current evidence supports the fact that immune cells, such as macrophages, natural killer (NK) cells, dendritic cells (DCs), neutrophils, T cells, and B cells, as well as cytokines and inflammatory mediators, contribute to the vascularization and fibrogenesis of endometriotic lesions, accelerating the implantation and development of ectopic endometrial lesions. Endocrine system dysfunction influences the immune microenvironment through overexpressed estrogen and progesterone resistance. In light of the limitations of hormonal therapy, we describe the prospects for potential diagnostic biomarkers and nonhormonal therapy based on the regulation of the immune microenvironment. Further studies are warranted to explore the available diagnostic biomarkers and immunological therapeutic strategies for endometriosis.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Uterine Diseases Uterine Diseases Uterine Diseases Uterine Diseases Uterine Diseases Biomarkers Biomarkers Biomarkers Biomarkers Biomarkers Estrogens Estrogens Estrogens Estrogens

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