Expression of PD-L1 in human placenta and retained product of conception of early pregnancy loss

Abstract

Abstract Introduction/Objective Immune surveillance evasion and impeding rejection by the maternal immune response system are elemental in sustaining foetal development. The exact mechanism behind this paradoxical immune response remains unclear. Since the trophoblast directly interacts with the maternal immune-environment, these cells must have some contribution to local immunosuppression. The programmed death-1 receptor and its ligands (PD- 1/PDL1)illustrates a novel regulatory-costulatory pathway that plays a major role in establishing peripheral tolerance. It was recently proved that PDL1 is expressed at the feto-maternal interface is necessary for maintaining feto-maternal tolerance. We undertook this study to determine the expression-pattern of PD-L1 in formalin-fixed paraffin embedded tissues of human placentas in third trimester and retained product in early spontaneous abortions. Methods/Case Report Clinical history were recorded. The H&E sections of 40 placenta & 20 RPOC cases were examined. After evaluation appropriate sections were selected for IHC examination using anti-PD-L1 antibodies of Lab-vision and Biogenic Results (if a Case Study enter NA) Main focus of study was to see expression of PD-L1 at feto-maternal interface. 30 out of 40 third-trimester placenta expressed PD-L1 immunohistochemistry (13, 11 and 6 cases showed intense, fair and weak positivity respectively on outer surface of syncytiotrophoblast). 2 out of 20 early pregnancy loss cases in 11 & 9wk gestation expressed PD-L1 positivity. Conclusion Fetal cells in direct contact with maternal blood villous syncytiotrophoblast are major source of PD-L1 at the maternal-fetal interface and may utilize these immuno-suppressive mechanisms to ensure tolerance of conceptus. Failure to adapt this mechanism can lead to pregnancy loss.