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Type: Journal article
Title: The majority of murine γδ T cells at the maternal-fetal interface in pregnancy produce IL-17
Other Titles: The majority of murine gamma delta T cells at the maternal-fetal interface in pregnancy produce IL-17
Author: Pinget, G.
Corpuz, T.
Stolp, J.
Lousberg, E.
Diener, K.
Robertson, S.
Sprent, J.
Webster, K.
Citation: Immunology and Cell Biology, 2016; 94(7):623-630
Publisher: Nature Publishing Group
Issue Date: 2016
ISSN: 0818-9641
Statement of
Gabriela V Pinget, Theresa M Corpuz, Jessica Stolp, Erin L Lousberg, Kerrilyn R Diener, Sarah A Robertson, Jonathan Sprent and Kylie E Webster
Abstract: Compared with lymphoid tissues, the immune cell compartment at mucosal sites is enriched with T cells bearing the γδ T-cell receptor (TCR). The female reproductive tract, along with the placenta and uterine decidua during pregnancy, are populated by γδ T cells predominantly expressing the invariant Vγ6(+)Vδ1(+) receptor. Surprisingly little is understood about the function of these cells. We found that the majority of γδ T cells in the non-pregnant uterus, pregnant uterus, decidua and placenta of mice express the transcription factor RORγt and produce interleukin-17 (IL-17). In contrast, IFNγ-producing γδ T cells were markedly reduced in gestational tissues compared with uterine-draining lymph nodes and spleen. Both uterine-resident invariant Vγ6(+) and Vγ4(+) γδ T cells which are more typically found in lymphoid tissues and circulating blood, were found to express IL-17. Vγ4(+) γδ T cells were particularly enriched in the placenta, suggesting a pregnancy-specific recruitment or expansion of these cells. A small increase in IL-17-producing γδ T cells was observed in allogeneic compared with syngeneic pregnancy, suggesting a contribution to regulating the maternal response to paternally-derived alloantigens. However, their high proportions also in non-pregnant uteri and gestational tissues of syngeneic pregnancy imply a role in the prevention of intrauterine infection or quality control of fetal development. These data suggest the need for a more rigorous evaluation of the role of IL-17 in sustaining normal pregnancy, particularly as emerging data points to a pathogenic role for IL-17 in pre-eclampsia, pre-term birth, miscarriage and maternal immune activation-induced behavioral abnormalities in offspring.
Keywords: Uterus
Mice, Inbred C57BL
Mice, Inbred DBA
Receptors, Antigen, T-Cell, gamma-delta
Maternal-Fetal Exchange
Nuclear Receptor Subfamily 1, Group F, Member 3
Rights: © 2016 Australasian Society for Immunology Inc. All rights reserved
DOI: 10.1038/icb.2016.48
Grant ID:
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