The Immunopathophysiology of Endometriosis

Lindsey K. Symons, Symons LK, Miller JE, Jessica E. Miller, Kay VR, Vanessa R. Kay, Ryan M. Marks, Marks RM, Kiera Liblik, Liblik K, Madhuri Koti, Koti M, Tayade C, Chandrakant Tayade
Trends in molecular medicine · 2018 · doi:10.1016/j.molmed.2018.07.004 · PMID:30054239
review OA: closed public-domain-us ⤵ 1 in-corpus citation
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This paper reviews current understanding of how immune dysfunction contributes to endometriosis and discusses future research directions for immune-based therapies.

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Abstract

Endometriosis is a chronic, inflammatory, estrogen-dependent disease characterized by the growth of endometrial tissue outside of the uterine cavity. Although the etiology of endometriosis remains elusive, immunological dysfunction has been proposed as a critical facilitator of ectopic lesion growth following retrograde menstruation of endometrial debris. However, it is not clear whether this immune dysfunction is a cause or consequence of endometriosis. Thus, here we provide in-depth insights into our current understanding of the immunopathophysiology of endometriosis and highlight challenges and opportunities for future research. With the explosion of successful immune-based therapies targeting various chronic inflammatory conditions, it is crucial to determine whether immune dysfunction can be therapeutically targeted in endometriosis.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Endometriosis Adaptive Immunity Animals Cytokines Cytokines Cytokines Endometriosis Endometriosis Endometrium Endometrium Endometrium Female Humans Immunity, Innate Inflammation Inflammation Inflammation Inflammation Neovascularization, Pathologic

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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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Courtesy of the U.S. National Library of Medicine