2012
DOI: 10.1093/humrep/des083
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Induction of endometriosis alters the peripheral and endometrial regulatory T cell population in the non-human primate

Abstract: Our data suggest that a reduction in peripheral Tregs may be a causative factor for endometriosis-associated infertility, while the increase in ectopic Treg expression may aid lesion development. Furthermore, endometriosis appears to disrupt Treg recruitment in both eutopic and ectopic endometrium.

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Cited by 46 publications
(41 citation statements)
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“…The failure to implant embryos associated with endometriosis was transferrable in the peritoneal fluid (PF) in rabbits (35), as well as in mice who received human endometriotic PF (36). Induction of endometriosis in the baboon has been shown to be associated with gradual but profound alterations in the endometrium over time (37), suggesting that inflammation and the immune system may be involved in these changes.…”
Section: Endometriosis and Infertility – What Is The Evidence?mentioning
confidence: 99%
“…The failure to implant embryos associated with endometriosis was transferrable in the peritoneal fluid (PF) in rabbits (35), as well as in mice who received human endometriotic PF (36). Induction of endometriosis in the baboon has been shown to be associated with gradual but profound alterations in the endometrium over time (37), suggesting that inflammation and the immune system may be involved in these changes.…”
Section: Endometriosis and Infertility – What Is The Evidence?mentioning
confidence: 99%
“…Lower numbers of Treg cells have been detected in the eutopic endometrium of a non-human primate endometriosis model [44]. Interestingly, in humans, the expression of the transcription factor forkhead P3 (Foxp3), a distinctive surface marker for Treg cells, is upregulated in the endometrium of women with endometriosis [45].…”
Section: Inflammation Immune Dysfunction and Infertilitymentioning
confidence: 99%
“…Patients with endometriosis have elevated levels of immune mediators in the peritoneal fluid, which is believed to occur as a result of improper ectopic tissue clearance [13][14][15]. Women with endometriosis have been shown to have reduced T regulatory cell populations in both the periphery and within the endometrium [16], as well as increased T regulatory cells in ectopic endometrial tissue [17], creating an immunosuppressive microenvironment that allows for endometriotic lesions to survive. Together, these data suggest endometriosis may be characterized as an immune disorder with autoimmune and chronic inflammatory tendencies.…”
Section: Introductionmentioning
confidence: 99%