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Publications

Journal Article Review Research Support, Non-U.S. Gov't Epublish 2 citations

PubMed: 39791759 DOI: 10.3390/cells14010058

The Estrogen-Immune Interface in Endometriosis.

Cells 14(1)

Authors: Emily Greygoose, Pat Metharom, Hakan Kula, Timur K Seckin, Tamer A Seckin, Ayse Ayhan, Yu Yu

Affiliations

  • Curtin Health Innovation Research Institute (CHIRI), Faculty of Health Sciences, Curtin University, Perth, WA 6102, Australia. Curtin Medical School, Faculty of Health Sciences, Curtin University, Perth, WA 6102, Australia.
  • Curtin Health Innovation Research Institute (CHIRI), Faculty of Health Sciences, Curtin University, Perth, WA 6102, Australia.
  • Curtin Medical School, Faculty of Health Sciences, Curtin University, Perth, WA 6102, Australia.
  • Department of Obstetrics and Gynecology, Faculty of Medicine, Dokuz Eylul University, Izmir 35340, Turkey.
  • Burnett School of Medicine, Texas Christian University, Fort Worth, TX 76104, USA.
  • Department of Gynecology, Lenox Hill Hospital, and Hofstra University, New York, NY 10075, USA.
  • Department of Tumor Pathology, Hamamatsu University School of Medicine, Hamamatsu 431-3192, Japan.
  • Department of Gynecology and Obstetrics, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
  • Discipline of Obstetrics and Gynaecology, Medical School, University of Western Australia, Crawley, WA 6009, Australia.

Abstract

Endometriosis is a gynecologic condition characterized by the growth of endometrium-like stroma and glandular elements outside of the uterine cavity. The involvement of hormonal dysregulation, specifically estrogen, is well established in the initiation, progression, and maintenance of the condition. Evidence also highlights the association between endometriosis and altered immune states. The human endometrium is a highly dynamic tissue that undergoes frequent remodeling in response to hormonal regulation during the menstrual cycle. Similarly, endometriosis shares this propensity, compounded by unclear pathogenic mechanisms, presenting unique challenges in defining its etiology and pathology. Here, we provide a lens to understand the interplay between estrogen and innate and adaptive immune systems throughout the menstrual cycle in the pathogenesis of endometriosis. Estrogen is closely linked to many altered inflammatory and immunomodulatory states, affecting both tissue-resident and circulatory immune cells. This review summarizes estrogenic interactions with specific myeloid and lymphoid cells, highlighting their implications in the progression of endometriosis.

MeSH

Endometriosis, Cells, Menstrual Cycle, Estrogens, Endometrium, Tissues

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