Peripheral and Endometrial Dendritic Cell Populations during the Normal Cycle and in the Presence of Endometriosis

David E Maridas, Alison J. Hey‐Cunningham, Alison J Hey-Cunningham, Cecilia Ng, Cecilia H M Ng, Robert Markham, Ian S Fraser, Marina Berbic
Journal of endometriosis and pelvic pain disorders · 2014 · vol. 6(2) , pp. 92–99 · doi:10.5301/je.5000180 · PMID:29354600 · W2048507323
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This study evaluated peripheral blood and endometrial dendritic cell populations, finding significant dysregulation in women with endometriosis compared to controls.

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Abstract

BACKGROUND: Dysfunctional immune response may be implicated in endometriosis pathogenesis, and dendritic cells (DC) may play greater roles in this response than previously recognized. This study set out to evaluate peripheral blood and endometrial DC population changes in the presence and absence of endometriosis pathology. METHODS: Endometrial (n = 83) and peripheral blood samples (n = 30) were subjected to immunohistochemical techniques and flow cytometry, respectively, to assess DC populations in women with and without endometriosis. Three circulating DC subsets (MDC1, MDC2 and PDC, expressing CD1c, CD303 and CD141), and late-stage mature endometrial DCs (using DC-LAMP antibody) were investigated. RESULTS: A highly significant reduction in CD1c intensity on MDC1 populations in peripheral blood was observed between normal cycle proliferative and menstrual phases (p = 0.025), but not in women with endometriosis, in whom CD1c intensity was markedly increased at the time of menstruation (p = 0.05). A significant reduction in peripheral blood MDC2 (p = 0.016) and apparent reduction in endometrial DC-LAMP+ DC (trend, p = 0.062) were observed in women with endometriosis compared with controls, consistent with our preliminary DC data. CONCLUSIONS: Cyclical variation in endometrial and circulating DC populations appears to be crucial during normal menstrual cycles and in the establishment of pregnancy. In endometriosis, circulating and endometrial DC populations are significantly dysregulated at a number of levels, and are likely to contribute to inefficient immunological targeting of endometrial fragments shed at menstruation, facilitating their survival and establishment of endometriosis.

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endometriosis

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