Document Detail

Maternal PD-1 regulates accumulation of fetal antigen-specific CD8+ T cells in pregnancy.
MedLine Citation:
PMID:  19368976     Owner:  NLM     Status:  MEDLINE    
The failure to reject the semi-allogeneic fetus suggests that maternal T lymphocytes are regulated by potent mechanisms in pregnancy. The T cell immunoinhibitory receptor, Programmed Death-1 (PD-1), and its ligand, B7-H1, maintain peripheral tolerance by inhibiting activation of self-reactive lymphocytes. Here, we investigated the role of the PD-1/B7-H1 pathway in maternal tolerance of the fetus. Antigen-specific maternal T cells both proliferate and upregulate PD-1 in vivo at mid-gestation in response to paternally inherited fetal antigen. In addition, when these cells carry a null deletion of PD-1, they accumulate excessively in the uterus-draining lymph nodes (P<0.001) without a concomitant increase in proliferation. In vitro assays showed that apoptosis of antigen-specific CD8(+) PD-1(-/-) cells was reduced following peptide stimulation, suggesting that the accumulation of these cells in maternal lymph nodes is due to decreased cell death. However, the absence of neither maternal PD-1 nor B7-H1 had detectable effects on gestation length, litter size, or pup weight at birth in either syngeneic or allogeneic pregnancies. These results suggest that PD-1 plays a previously unrecognized role in maternal-fetal tolerance by inducing apoptosis of paternal antigen-specific T cells during pregnancy, thereby controlling their abundance.
Elizabeth S Taglauer; Thomas M Yankee; Margaret G Petroff
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2009-04-14
Journal Detail:
Title:  Journal of reproductive immunology     Volume:  80     ISSN:  1872-7603     ISO Abbreviation:  J. Reprod. Immunol.     Publication Date:  2009 Jun 
Date Detail:
Created Date:  2009-06-01     Completed Date:  2010-05-13     Revised Date:  2014-04-10    
Medline Journal Info:
Nlm Unique ID:  8001906     Medline TA:  J Reprod Immunol     Country:  Ireland    
Other Details:
Languages:  eng     Pagination:  12-21     Citation Subset:  IM    
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MeSH Terms
Antigens, Differentiation / genetics,  immunology,  metabolism*
Apoptosis / genetics,  immunology
CD8-Positive T-Lymphocytes / immunology,  metabolism*,  pathology
Cell Movement / immunology
Fetal Development / genetics,  immunology
Histocompatibility / genetics,  immunology*
Histocompatibility Antigens / immunology*
Litter Size / genetics,  immunology
Lymph Nodes / pathology
Lymphocyte Activation / genetics
Mice, Inbred BALB C
Mice, Inbred C57BL
Mice, Knockout
Mice, Transgenic
Ovalbumin / immunology
Pregnancy, Animal / immunology*
Signal Transduction / immunology
Grant Support
HD049480/HD/NICHD NIH HHS; HD45611/HD/NICHD NIH HHS; P01 HD049480-020003/HD/NICHD NIH HHS; P20 RR017686/RR/NCRR NIH HHS; P20 RR017686-045684/RR/NCRR NIH HHS; P20 RR024214-02/RR/NCRR NIH HHS; P20RR016475/RR/NCRR NIH HHS; P20RR017686/RR/NCRR NIH HHS; P20RR024214/RR/NCRR NIH HHS; R01 HD045611/HD/NICHD NIH HHS; R01 HD045611-06/HD/NICHD NIH HHS
Reg. No./Substance:
0/Antigens, Differentiation; 0/Histocompatibility Antigens; 0/Pdcd1 protein, mouse; 9006-59-1/Ovalbumin

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