Maternal CXCR4 deletion results in placental defects and pregnancy loss mediated by immune dysregulation
Ontology highlight
ABSTRACT: The pregnant decidua is infiltrated by many immune cells which are thought to originate in the bone marrow (BM) promoting pregnancy. CXCR4 is a key regulator of the development of NK cells and dendritic cells, both of which play an important role in early placental development and immune tolerance at the maternal-fetal interface. However, the role of CXCR4 in pregnancy is not well understood. To generate tamoxifen-inducible CXCR4 knockout mice, we used the Cre/LoxP tamoxifen-inducible system. For animal experiments, Cre+/CXCR4fl/fl mice and their Cre-/CXCR4fl/fl littermates were used. After tamoxifen treatment, we refer to Cre-/CXCR4fl/wt mice as WT (wild type), and Cre+/CXCR4fl/null mice as CXCR4 KO (knockout). For adoptive bone marrow transplant (BMT) experiments, BMT was performed from either WT GFP transgenic male donor mice into WT or CXCR4 KO females, or from CXCR4 KO male donors into CXCR4 KO females as negative control. Collectively, our study found an important role for maternal CXCR4 expression in immune cell function, placental development and pregnancy maintenance.
ORGANISM(S): Mus musculus
PROVIDER: GSE241958 | GEO | 2023/12/20
REPOSITORIES: GEO
ACCESS DATA