期刊
FRONTIERS IN IMMUNOLOGY
卷 7, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2016.00043
关键词
mouse models; uterine NK cells; placenta; pregnancy; lymphocyte subpopulations
类别
资金
- Wellcome Trust [094073/Z/10/Z]
- Leukaemia and Lymphoma Research [13010]
- Centre for Trophoblast Research
- British Heart Foundation [FS/12/4/29254]
- Cambridge NIHR BRC Cell Phenotyping Hub
- Marie Curie FP7 Fellowship
- Centre for Trophoblast Research Graduate Studentship
- MRC [G0901737] Funding Source: UKRI
- Wellcome Trust [094073/Z/10/Z] Funding Source: Wellcome Trust
- British Heart Foundation [FS/12/4/29254, PG/09/077/27964] Funding Source: researchfish
- Medical Research Council [G0901737] Funding Source: researchfish
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.
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