Abstract
The programmed cell death protein 1 (PD-1) receptor has been reported to downregulate T cell activation effectively via binding to its ligands PD-L1 or PD-L2 in a negative co-stimulatory manner. Little is known about the involvement of PD-1 mediated immunoregulation in pregnancy and in pregnancy-related disorders. In this work, we investigated the possible role of the PD-1 co-stimulatory pathway in the pathogenesis of the clinical phase of early-onset preeclampsia characterized by a systemic maternal inflammatory response. We performed a cross-sectional study for comparative analysis of phenotypic and functional characteristics of peripheral blood mononuclear cells in women with early-onset preeclampsia and third-trimester healthy pregnant controls. According to our findings, enhanced expression of either PD-1 or its ligand PD-L1, or both, on the cell surface of effector cells (T cells, natural killer (NK) cells, natural killer T (NKT)-like cells) and Tregs could be observed, but PD-1 expression did not correlate with effector cells exhaustion. These results suggest the failure of the axis to downregulate Th1 responses, contributing thereby to the exaggerated immunoactivation observed in early-onset preeclampsia.
Highlights
From an immunological point of view, pregnancy is considered to represent a permanent challenge for the maternal immune system, maintaining a delicate balance between protective immunity and tolerance [1]
We investigated the possible role of the programmed death-1 (PD-1) co-stimulatory pathway in the pathogenesis of the clinical phase of early-onset preeclampsia analyzing phenotypic and functional characteristics of peripheral blood lymphocytes
We determined the ratio of different lymphocyte subpopulations in the peripheral blood of healthy pregnant and early-onset preeclamptic women
Summary
From an immunological point of view, pregnancy is considered to represent a permanent challenge for the maternal immune system, maintaining a delicate balance between protective immunity and tolerance [1]. Thereby, a major role was referred to immunoregulatory mechanisms overwriting ongoing immunoactivation both on a cellular (e.g., regulatory T cells (Treg)) and on a molecular (e.g., inhibitory receptors) level. The actual hypothesis of successful T cell activation suggests the involvement of multiple incoming signals beside T-cell receptor (TCR) dependent recognition of the Major histocompatibility complex (MHC)-antigen complex [2,3,4]. Some of these signals are delivered by immune checkpoint molecules with negative regulatory potential. The programmed death-1 (PD-1) receptor is a 55 kDa transmembrane protein belonging to the Ig superfamily [5,6].
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: 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.
