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The involvement of multifunctional TGF-β and related cytokines in pathogenesis of endometriosis.

Abstract：

PURPOSE:Transforming growth factor β (TGF-β) is one of the major immune and inflammation factors responsible for regulating cell proliferation, differentiation, angiogenesis, and immune responses. Deregulated TGF-β activity, especially its influence in peritoneal cytokine cross-talk, has been implicated in pathologies of endometriosis. The aim of this study was to determine whether TGF-β could be involved in the pathogenesis of endometriosis. For this purpose, we evaluated concentrations of TGFβ1, TGF-β2, TGF-β3 and interleukin (IL)-1β, IL-6, IL-10, IL-17, IL-21 and IL-22 in peritoneal fluid (PF) and serum of women with endometriosis. METHODS:A total of 66 women of reproductive age were involved in the study, 51 endometriosis patients, and 15 women from the control group. PF and serum levels of all cytokines were measured with ELISA in women with or without endometriosis. RESULTS:Higher PF and serum levels of TGF-β1, TGF-β2, TGF-β3, presented also as a total TGF-β in women with endometriosis compared to control were observed. The biggest increase was measured in the case of TGF-β1. The higher levels of IL-1β, IL-6, IL-10, and IL-17 in PF and serum of endometriosis women than control was observed. Higher PF levels of studied parameters in comparison with serum levels were found. CONCLUSIONS:In endometriosis, TGF-β could affect differentiation of T helper (Th) cells, hence produce more IL-17 and IL-10 to PF and might have an indirect influence on inflammation, which is associated with higher IL-1β and IL-6 levels. In consequent, TGF-β in peritoneal fluid may promote an environment favorable to ectopic lesion formation.

journal_name

Immunol Lett

journal_title

Immunology letters

authors

Sikora J,Smycz-Kubańska M,Mielczarek-Palacz A,Bednarek I,Kondera-Anasz Z

doi

10.1016/j.imlet.2018.10.011

subject

Has Abstract

pub_date

2018-09-01 00:00:00

pages

31-37

eissn

0165-2478

issn

1879-0542

pii

S0165-2478(18)30353-5

journal_volume

201

pub_type

杂志文章

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