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The programmed death-1 (PD-1)/PD-L1 pathway plays important roles in immune responses and peripheral tolerance. Under pathological conditions, this pathway can suppress protective T cell responses and induce immune system disorders. Endometriosis (EM) is an estrogen-dependent, immune-associated disease. The expression of PD-1 and PD-L1 has been studied in a variety of cancers and autoimmune diseases. Few studies, however, have attempted to explore their expression and the possibility that they are regulated by estrogen in EM. Eutopic and ectopic endometria and blood samples were collected from 15 women with EM and 15 women without EM. PD-1/PD-L1 expression in endometrial tissues was detected using immunohistochemistry and western blot analysis. Their expression in blood was detected using flow cytometry. In addition, their expression was evaluated in endometrial cells after estrogen and cytokine treatment. We observed PD-1/PD-L1 expression in both eutopic and ectopic endometria, with elevated expression in EM. Their expression was also higher in CD4+/CD8+ T cells in blood from EM patients. In addition, treatment with 17β-estradiol upregulated PD-L1 expression in eutopic epithelial cells in EM. These data suggest that the PD-1/PD-L1 pathway may be involved in EM immune dysfunction and be regulated by estrogen. [ABSTRACT FROM AUTHOR]

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Objective. To explore the stroma–epithelium interactions in endometriosis and to identify the possible signalling pathways involved in this cross-talk. Design. Laboratory study via primary cultured endometrial stromal and epithelial cells. Setting. University Hospital. Patients. Fifteen patients with endometriosis confirmed by histopathology were recruited in the study, and 12 women free of endometriosis were used as control group. Intervention(s). Specific NFкB inhibitor 1-Pyrrolidinecarbodithioic acid ammonium salt (PDTC) was used in cell cultures. Main outcome measure(s). The expression and secretion of MMP-2, MMP-9, TIMP-1, TIMP-2 and the DNA-binding activity of NFкB in normal endometrial stromal cells or in co-cultures with normal or endometriotic epithelial cells from patients with endometriosis. Result(s). Endometrial epithelial cells induced MMP-9 and MMP-2 expression in normal stromal cells in vitro. In co-cultures with endometriotic epithelial cells, normal endometrial stromal cells expressed and secreted higher MMP-2 ( p < 0.05) and MMP-9 ( p < 0.05). Specific inhibition of NFкB pathway in stromal cells abolished this induction effect by epithelial cells. Conclusion(s). Endometriotic epithelial cells induce MMPs expression and secretion in normal endometrial stromal cells via an NFкB-dependent pathway in vitro. This cross-talk between epithelial cells and stromal cells may facilitate the implantation and extension of the ectopic foci and favour the development of the disease. [ABSTRACT FROM AUTHOR]