Endometriosis associated with defective handling of apoptotic cells in the female genital tract is a major cause of autoimmune disease in women

John P. Seery, Seery JP
Medical hypotheses · 2006 · vol. 66(5) , pp. 945–949 · doi:10.1016/j.mehy.2005.11.032 · PMID:16412582 · W2014044639
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This paper examines the role of defective handling of apoptotic cells in the female genital tract as a significant factor contributing to autoimmune disease in women with endometriosis.

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Abstract

Several autoimmune diseases are far more common in women than men. The reasons are unknown. Recent studies have shown that many autoimmune diseases which predominantly affect females are characterized by the production of autoantibodies against components of apoptotic cells. Furthermore, in experimental animals, defective clearance of apoptotic cells in a pro-oxidant inflammatory environment can trigger the production of these autoantibodies and related autoimmune disease. Endometriosis is characterized by defective clearance of apoptotic endometrial cells in a pro-oxidant inflammatory environment. It is proposed that this combination of abnormalities triggers autoantibody production in women affected by endometriosis. A proportion of these women will be genetically predisposed to develop overt autoimmune disease. As endometriosis affects at least 4% of the female population of reproductive age, this phenomenon will have a major effect on the gender prevalence of several related autoimmune syndromes. The hypothesis is supported by epidemiological studies which show a strong association between endometriosis and female-predominant autoimmune disorders.

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Condition tags

endometriosis

MeSH descriptors

Apoptosis Autoimmune Diseases Autoimmune Diseases Endometriosis Endometriosis Genitalia, Female Apoptosis Apoptosis Autoimmune Diseases Autoimmune Diseases Causality Causality Clinical Trials as Topic Clinical Trials as Topic Comorbidity Comorbidity Endometriosis Endometriosis Evidence-Based Medicine Evidence-Based Medicine

Citation neighborhood (2-hop)

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. Outer rings show 2-hop neighbours — papers reached through the immediate citers/citees. [ collapse to 1-hop ]

References (43)

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