{"paper_id":"5fc63a01-0a8a-43c8-ad53-862ad9af529b","body_text":"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.\nelevated ERβ levels in endometriotic tissue disrupt apoptosis complex I, apoptosis complex II and apoptosome formation\nThis is a preview of subscription content, access via your institution\nAccess options\nSubscribe to this journal\nReceive 12 print issues and online access\n251,40 € per year\nonly 20,95 € per issue\nBuy this article\n- Purchase on SpringerLink\n- Instant access to the full article PDF.\n39,95 €\nPrices may be subject to local taxes which are calculated during checkout\nReferences\nHan, S. J. et al. Estrogen receptor β modulates apoptosis complexes and the inflammasome to drive the pathogenesis of endometriosis. Cell 163, 960–974 (2015)\nRights and permissions\nAbout this article\nCite this article\nLeavy, O. Evading immunosurveillance in endometriosis. Nat Rev Immunol 15, 729 (2015). https://doi.org/10.1038/nri3942\nPublished:\nIssue date:\nDOI: https://doi.org/10.1038/nri3942","source_license":"CC0","license_restricted":false}