Evading immunosurveillance in endometriosis

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AI-generated summary by claude@2026-07+body, 2026-07-16

Elevated ERβ expression in mouse endometriotic tissue disrupts apoptosis, increasing lesion volume and cell proliferation while reducing apoptosis.

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The paper reports that, in a mouse model of endometriosis, estrogen receptor beta (ERβ) expression and activity are greatly increased in ectopic lesions compared with normal endometrium. Loss of ERβ reduced ectopic lesion volume, decreased cell proliferation, and increased apoptosis, whereas ERβ overexpression had the opposite effects. Mechanistically, elevated ERβ levels disrupted apoptosis complex I, apoptosis complex II, and apoptosome formation in endometriotic tissue. This paper is centrally about endometriosis—specifically how ERβ regulates apoptosis and lesion growth in endometriosis.

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The authors first confirmed that, in mouse endometriotic tissue, the expression and activity of ERβ is greatly increased compared with normal endometria. Loss of ERβ expression decreased ectopic lesion volume, reduced cell proliferation and increased apoptosis in mouse endometriotic tissue. By contrast, overexpression of ERβ increased lesion volume and cell proliferation, and decreased apoptosis. elevated ERβ levels in endometriotic tissue disrupt apoptosis complex I, apoptosis complex II and apoptosome formation This is a preview of subscription content, access via your institution Access options Subscribe to this journal Receive 12 print issues and online access 251,40 € per year only 20,95 € per issue Buy this article - Purchase on SpringerLink - Instant access to the full article PDF. 39,95 € Prices may be subject to local taxes which are calculated during checkout References Han, S. J. et al. Estrogen receptor β modulates apoptosis complexes and the inflammasome to drive the pathogenesis of endometriosis. Cell 163, 960–974 (2015) Rights and permissions About this article Cite this article Leavy, O. Evading immunosurveillance in endometriosis. Nat Rev Immunol 15, 729 (2015). https://doi.org/10.1038/nri3942 Published: Issue date: DOI: https://doi.org/10.1038/nri3942

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Estrogen Receptor beta Inflammasomes Menstruation Animals Endometriosis Estrogen Receptor beta Female Humans Inflammasomes Menstruation

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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