Abstract
Introduction: Programmed death-1 (PD-1) is one of the most important inhibitory co-receptors. Studies show that the PD-1/PD-L1 pathway regulates the induction and maintenance of peripheral tolerance and protects tissues from attack in physiological conditions. Several studies have shown association of PD-1/PD-L1 pathway with several diseases although, to date, no such studies have been performed for endometriosis. Aims: The aim of this study was to describe the frequencies of T and B lymphocytes expressing PD-1 and PD-L1 molecules in patients with endometriosis. Material and methods: The expression of PD-1 and PD-L1 was analyzed using flow cytometry on T and B lymphocytes collected from 20 adult women with newly diagnosed, untreated endometriosis. The control group consisted of 20 healthy age-matched women. Results: We observed high expression of PD-1 and PD-L1 on analyzed lymphocytes subpopulations of patients with endometriosis. Among T cells, the expression of PD-1 on protein level was higher on CD4+ cells in patients (mean: 31.54 ± 13.74%) than in healthy controls (mean: 5.35 ± 1.54%, p < 0.001). Moreover, higher frequencies of PD-1 + /CD8 + cells and PD-1 + /CD19 + cells in the study group than in healthy volunteers were observed (mean: 18.71 ± 10.37% vs. 3.6 ± 1.45%, p = 0.015 and 12.07 ± 4.34% vs. 1.67 ± 0.84%, p = 0.017, respectively). There was a positive correlation between PD-1 + and PD-L1 + CD19 + B cells (r = 0.43, p = 0.026). Conclusion: High expression of PD-1 and PD-L1 on T and B cells could represent the hallmark of immune system reaction to chronic antigenic exposition in patients with endometriosis.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
More From: European Journal of Obstetrics & Gynecology and Reproductive Biology
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.