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Genetic deletion of Cxcl14 in mice alters uterine NK cells
- Cao, Qichen, Chen, Hua, Deng, Zhili, Yue, Jingwen, Chen, Qi, Cao, Yujing, Ning, Lina, Lei, Xiaohua, Duan, Enkui
- Biochemical and biophysical research communications 2013 v.435 pp. 664-670
- secretion, placenta, immunosuppression, microarray technology, cytokines, mice, pregnancy, bone marrow, genes, knockout mutants, population growth, natural killer cells, spleen, uterus, embryogenesis, gene expression regulation, angiogenesis
- The uterine natural killer cells (uNK cells) are the major immune cells in pregnant uterus and the number of uNK cells is dramatically increased during placentation and embryo development. The uNK cells are necessary for the immune tolerance, cytokine secretion and angiogenesis of placenta. Former studies indicated that the population expansion of uNK cells was accomplished through recruitment of NK cell precursors from the spleen and bone marrow, but not proliferation of NK cells. However, the necessary molecules within this process were little understood. Here in our study, we found the co-localized expression of Cxcl14 protein with uNK cells in E13.5 pregnant uterus. Moreover, we used Cxcl14 knockout mice to examine uNK cells in mesometrial lymphoid aggregate of pregnancy (MLAp) and decidua basalis (DB) of E13.5 pregnant uterus and found significantly decreased uNK cells in Cxcl14−/− pregnant uteri compared with Cxcl14+/− pregnant uteri. To further explorer the molecular change in MLAp and DB after Cxcl14 knockout, we isolated the MLAp and DB from Cxcl14+/+ and Cxcl14−/− pregnant uteri and performed microarray analysis. We found many genes were up and down regulated after Cxcl14 knockout. In conclusion, our results suggested the important function of Cxcl14 in uNK cells and the proper level of Cxcl14 protein were required to recruit NK cells to pregnant uterus.