Role of PD1/PDL1 pathway, and TH17 and treg cells in maternal tolerance to the fetus

Biomed J. Jan-Feb 2015;38(1):25-31. doi: 10.4103/2319-4170.143511.

Abstract

Tolerance of the fetus by the maternal immune system is regulated through various mechanisms involving the different immune cells, both in the periphery and locally at the feto-maternal interface. The maternal T lymphocytes are aware of the paternal fetal antigens and a state of dynamic T cell homeostasis is maintained in the uterus during gestation, which involves increase in antigen-specific regulatory T cell (Treg) proliferation, increase in apoptosis of antigen-specific effector T cells, and inhibition of excessive inflammation post successful implantation to ensure tolerance to the fetus. The Tregs play an important role in the maintenance of tolerance during gestation. Recently, the inflammatory T helper type 17 (Th17) cells are reported to have a role in loss of tolerance to the fetus. The interaction between costimulatory molecule programmed death 1 (PD1) and its ligand PDL1 is known to play a role in regulating both the Tregs and Th17 cells. Here we discuss how the PD1/PDL1 pathway affects these two T cell populations and its role in feto-maternal tolerance.

Publication types

  • Review

MeSH terms

  • Animals
  • B7-H1 Antigen / immunology*
  • Fetus / immunology*
  • Humans
  • Immune Tolerance / immunology*
  • Programmed Cell Death 1 Receptor / immunology*
  • T-Lymphocytes, Regulatory / cytology*
  • T-Lymphocytes, Regulatory / immunology
  • Th17 Cells / cytology*
  • Th17 Cells / immunology

Substances

  • B7-H1 Antigen
  • CD274 protein, human
  • PDCD1 protein, human
  • Programmed Cell Death 1 Receptor