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Expression and Function of PDCD1 at the Human Maternal-Fetal Interface¹

Department of Anatomy and Cell Biology,³ and Microbiology, Molecular Genetics and Immunology, ⁴ University of Kansas Medical Center, Kansas City, Kansas 66160 University of Kansas,⁵ Lawrence, Kansas 66045

ABSTRACT

The failure to reject the semiallogenic fetus by maternal T lymphocytes suggests that potent mechanisms regulate these cells. PDCD1 is a CD28 family receptor expressed by T cells, and its ligand CD274 is strongly expressed by trophoblast cells of the human placenta. In this study, we examined whether human maternal T cells express PDCD1. Immunofluorescence examination of uterine tissues revealed PDCD1 expression on CD3⁺ cells was low in nonpregnant endometrium but increased in first-trimester decidua and remained elevated in term decidua (P < 0.05). In addition, higher relative proportions of term decidual CD8^bright, CD4⁺, and regulatory T cells expressed PDCD1 in comparison to autologous peripheral blood (P < 0.05). Term decidual T cells also expressed full-length and soluble PDCD1 mRNA isoforms more abundantly than their peripheral blood counterparts (P 0.05). We also examined the effects of PDCD1:CD274 interactions in decidual T cells. Jar choriocarcinoma cells were transfected with CD274 and cocultured with activated decidual CD4⁺ or CD8^bright T cells for 72 h followed by analysis of cytokine concentration and decidual T cell apoptosis. Compared with empty vector-transfected cells, CD274-transfected Jar cells caused a significant suppression of interferon gamma and tumor necrosis factor alpha production by CD4⁺ (P < 0.05) but not CD8^bright T cells, while having no effect on secretion of IL10 or T cell apoptosis. These results suggest that the PDCD1:CD274 pathway functions in modification of maternal decidual lymphocyte cytokine secretion during pregnancy.

B7-H1, CD274, CD279, decidua, PD-1, PDL1, PDCD1, placenta, T cells

¹ Supported by National Institutes of Health grants HD45611 to M.G.P. and HD049480 to M.G.P., director of Project II; C. Ober, director of Tissue Collection Core, and J.S. Hunt, principal investigator. E.S.T. was supported by a fellowship from the University of Kansas Medical Center (KUMC) Biomedical Research Training Program. Further resources and services were provided by the KUMC for Reproductive Sciences (NICHD), the KUMC Flow Cytometry Core (NCRR), the KUMC COBRE program in Cell Development and Differentiation (P20RR024214), the Kansas State University COBRE program in Epithelial Function (P20RR017686), the Kansas Idea Network of Biomedical Research Excellence (P20RR016475), and the Smith Intellectual and Developmental Disabilities Research Center (HD02528).

Correspondence: ²Margaret G. Petroff, Department of Anatomy and Cell Biology, University of Kansas Medical Center, 3901 Rainbow Blvd., Mail Stop 3038, Kansas City, KS 66160-7400. FAX: 913 588 7180; e-mail: mpetroff{at}kumc.edu