Exacerbation of endometriosis due to regulatory T cell dysfunction.

Exacerbation of endometriosis due to regulatory T cell dysfunction.

J Clin Endocrinol Metab. 2017 May 26;:

Authors: Tanaka Y, Mori T, Ito F, Koshiba A, Takaoka O, Kataoka H, Maeda E, Okimura H, Mori T, Kitawaki J

Abstract
Context: Endometriosis is a chronic inflammatory disease associated with altered immune response to endometrial cells facilitating the implantation and proliferation of ectopic endometrial tissues. Although regulatory T (Treg) cells play a key role in T cell-mediated immune response and development of immune disorders, their significance in endometriosis remains to be elucidated. Recently, CD4+CD45RA- forkhead box protein 3 (Foxp3)hi T cells, activated Treg cells, have been identified as a functionally true suppressive population of Treg cells.
Objective: To investigate the role of Treg cells in endometriosis.
Design: Three Treg cell fractions (resting Treg cells, activated Treg cells, and non-Treg cells) were examined using flow cytometry in the endometrioma, endometrium, peritoneal fluid, and peripheral blood obtained from women with (n = 27) and without (n = 28) endometriosis. A mouse model of endometriosis was made in Foxp3tm3Ayr/J (Foxp3DTR) C57BL/6 Treg cell-depleted mice (n = 28).
Results: In women with endometrioma, the proportion of activated Treg cells in the endometrioma and the endometrium, but not in the peritoneal fluid or peripheral blood, was significantly decreased compared with that in women without endometriosis. In Foxp3DTR/ diphtheria toxin (DT) mice, the number and weight of endometriotic lesions, inflammatory cytokine levels and angiogenetic factors were significantly increased compared with those in control mice.
Conclusions: Treg cell deficiency exaggerates local inflammation and angiogenesis and simultaneously facilitates the attachment and growth of endometrial implants. The findings provide a novel insight into dysregulated immune response for the pathogenesis and development.

PMID: 28575420 [PubMed - as supplied by publisher]

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