Immunotherapy: A promising novel endometriosis therapy

Wenshu Li, Aimin Lin, Lin Qi, Xin Lv, Shenghuan Yan, Jing Xue, Xuefang Jing, Nan Mu
Frontiers in immunology · 2023 · vol. 14 , pp. 1128301 · doi:10.3389/fimmu.2023.1128301 · PMID:37138868 · W4366221058
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

This review examines immunomodulators targeting immune cells and factors, suggesting immunotherapy may be a novel and effective treatment option for endometriosis due to its potential to inhibit lesion development.

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

This paper reviews evidence on how abnormal immune function contributes to endometriosis pathogenesis and evaluates immunomodulators as potential therapies by targeting immune cells (neutrophils, macrophages, NK cells, T cells, mast cells, dendritic cells) and immune factors/signaling pathways. It reports that, compared with healthy controls, patients show increased neutrophil and macrophage presence and altered activities such as heightened neutrophil aggregation, macrophage dysfunction with attenuated phagocytosis, reduced NK cytotoxicity, and T-cell subset shifts (including increased Tregs), which together may enable immune escape, lesion survival, inflammation, angiogenesis, pelvic pain, and recurrence; it also notes that immunotherapy information for clinical application remains limited. A major limitation is that the article is a narrative review, and it explicitly calls for detailed mechanistic experimental work and large-scale clinical studies to establish effectiveness and safety. This paper is centrally about endometriosis — it specifically reviews immunotherapy strategies aimed at immune dysregulation in endometriosis.

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Abstract

Endometriosis is a common disease of the female reproductive system and has malignant features. Although endometriosis by itself is a benign disease, its erosive growth characteristics lead to severe pelvic pain and female infertility. Unfortunately, several aspects of the pathogenesis of endometriosis are still unclear. Furthermore, the clinical therapeutic methods are unsatisfactory. The recurrence rate of endometriosis is high. Accumulating evidence suggests that the onset and development of endometriosis are closely related to the abnormal function of the female autoimmune system, especially the function of some immune cells such as the aggregation of neutrophils, abnormal differentiation of macrophages, decreased cytotoxicity of NK cells, and abnormal function of T- and B-cell lines. Therefore, immunotherapy is probably a novel therapeutic strategy for endometriosis besides surgery and hormone therapy. However, information regarding the clinical application of immunotherapy in the treatment of endometriosis is very limited. This article aimed to review the effects of existing immunomodulators on the development of endometriosis, including immune cell regulators and immune factor regulators. These immunomodulators clinically or experimentally inhibit the pathogenesis and development of endometriosis lesions by acting on the immune cells, immune factors, or immune-related signaling pathways. Thus, immunotherapy is probably a novel and effective clinical treatment choice for endometriosis. Experimental studies of the detailed mechanism of immunotherapy and large-scale clinical studies about the effectiveness and safety of this promising therapeutic method are required in the future.

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Condition tags

mesh:D004715endometriosisinfertility

MeSH descriptors

Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Infertility, Female

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 (93)

Cited by (25)

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