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The Residual Innate Lymphoid Cells in NFIL3-Deficient Mice Support Suboptimal Maternal Adaptations to Pregnancy
Uterine NK cells are innate lymphoid cells (ILC) that populate the uterus and expand during pregnancy, regulating placental development and fetal growth in humans and mice. We have recently characterized the composition of uterine ILCs (uILCs), some of which require the transcription factor NFIL3, b...
Autores principales: | , , , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4759249/ https://www.ncbi.nlm.nih.gov/pubmed/26925058 http://dx.doi.org/10.3389/fimmu.2016.00043 |
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author | Boulenouar, Selma Doisne, Jean-Marc Sferruzzi-Perri, Amanda Gaynor, Louise M. Kieckbusch, Jens Balmas, Elisa Yung, Hong Wa Javadzadeh, Shagayegh Volmer, Léa Hawkes, Delia A. Phillips, Keli Brady, Hugh J.M. Fowden, Abigail L. Burton, Graham J. Moffett, Ashley Colucci, Francesco |
author_facet | Boulenouar, Selma Doisne, Jean-Marc Sferruzzi-Perri, Amanda Gaynor, Louise M. Kieckbusch, Jens Balmas, Elisa Yung, Hong Wa Javadzadeh, Shagayegh Volmer, Léa Hawkes, Delia A. Phillips, Keli Brady, Hugh J.M. Fowden, Abigail L. Burton, Graham J. Moffett, Ashley Colucci, Francesco |
author_sort | Boulenouar, Selma |
collection | PubMed |
description | Uterine NK cells are innate lymphoid cells (ILC) that populate the uterus and expand during pregnancy, regulating placental development and fetal growth in humans and mice. We have recently characterized the composition of uterine ILCs (uILCs), some of which require the transcription factor NFIL3, but the extent to which NFIL3-dependent cells support successful reproduction in mice is unknown. By mating Nfil3(−/−) females with wild-type males, here we show the effects of NFIL3 deficiency in maternal cells on both the changes in uILCs during pregnancy and the downstream consequences on reproduction. Despite the presence of CD49a(+)Eomes(−) uILC1s and the considerable expansion of residual CD49a(+)Eomes(+) tissue-resident NK cells and uILC3s in pregnant Nfil3(−/−) mice, we found incomplete remodeling of uterine arteries and decidua, placental defects, and fetal growth restriction in litters of normal size. These results show that maternal NFIL3 mediates non-redundant functions in mouse reproduction. |
format | Online Article Text |
id | pubmed-4759249 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-47592492016-02-26 The Residual Innate Lymphoid Cells in NFIL3-Deficient Mice Support Suboptimal Maternal Adaptations to Pregnancy Boulenouar, Selma Doisne, Jean-Marc Sferruzzi-Perri, Amanda Gaynor, Louise M. Kieckbusch, Jens Balmas, Elisa Yung, Hong Wa Javadzadeh, Shagayegh Volmer, Léa Hawkes, Delia A. Phillips, Keli Brady, Hugh J.M. Fowden, Abigail L. Burton, Graham J. Moffett, Ashley Colucci, Francesco Front Immunol Immunology Uterine NK cells are innate lymphoid cells (ILC) that populate the uterus and expand during pregnancy, regulating placental development and fetal growth in humans and mice. We have recently characterized the composition of uterine ILCs (uILCs), some of which require the transcription factor NFIL3, but the extent to which NFIL3-dependent cells support successful reproduction in mice is unknown. By mating Nfil3(−/−) females with wild-type males, here we show the effects of NFIL3 deficiency in maternal cells on both the changes in uILCs during pregnancy and the downstream consequences on reproduction. Despite the presence of CD49a(+)Eomes(−) uILC1s and the considerable expansion of residual CD49a(+)Eomes(+) tissue-resident NK cells and uILC3s in pregnant Nfil3(−/−) mice, we found incomplete remodeling of uterine arteries and decidua, placental defects, and fetal growth restriction in litters of normal size. These results show that maternal NFIL3 mediates non-redundant functions in mouse reproduction. Frontiers Media S.A. 2016-02-19 /pmc/articles/PMC4759249/ /pubmed/26925058 http://dx.doi.org/10.3389/fimmu.2016.00043 Text en Copyright © 2016 Boulenouar, Doisne, Sferruzzi-Perri, Gaynor, Kieckbusch, Balmas, Yung, Javadzadeh, Volmer, Hawkes, Phillips, Brady, Fowden, Burton, Moffett and Colucci. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Immunology Boulenouar, Selma Doisne, Jean-Marc Sferruzzi-Perri, Amanda Gaynor, Louise M. Kieckbusch, Jens Balmas, Elisa Yung, Hong Wa Javadzadeh, Shagayegh Volmer, Léa Hawkes, Delia A. Phillips, Keli Brady, Hugh J.M. Fowden, Abigail L. Burton, Graham J. Moffett, Ashley Colucci, Francesco The Residual Innate Lymphoid Cells in NFIL3-Deficient Mice Support Suboptimal Maternal Adaptations to Pregnancy |
title | The Residual Innate Lymphoid Cells in NFIL3-Deficient Mice Support Suboptimal Maternal Adaptations to Pregnancy |
title_full | The Residual Innate Lymphoid Cells in NFIL3-Deficient Mice Support Suboptimal Maternal Adaptations to Pregnancy |
title_fullStr | The Residual Innate Lymphoid Cells in NFIL3-Deficient Mice Support Suboptimal Maternal Adaptations to Pregnancy |
title_full_unstemmed | The Residual Innate Lymphoid Cells in NFIL3-Deficient Mice Support Suboptimal Maternal Adaptations to Pregnancy |
title_short | The Residual Innate Lymphoid Cells in NFIL3-Deficient Mice Support Suboptimal Maternal Adaptations to Pregnancy |
title_sort | residual innate lymphoid cells in nfil3-deficient mice support suboptimal maternal adaptations to pregnancy |
topic | Immunology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4759249/ https://www.ncbi.nlm.nih.gov/pubmed/26925058 http://dx.doi.org/10.3389/fimmu.2016.00043 |
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