Deletion of atypical chemokine receptor 3 (ACKR3) increases immune cells at the fetal-maternal interface.

ABSTRACT: Establishment of immune cell populations and adaptations in immune cells are critical aspects during pregnancy that lead to protection of the semi-allogenic fetus. Appropriate immune cell activation and trophoblast migration are regulated in part by chemokines, the availability of which can be fine-tuned by decoy receptors. Atypical chemokine receptor 3 (ACKR3), previously named C-X-C chemokine receptor 7 (CXCR7), is a chemokine decoy receptor expressed in placenta, but little is known about how this receptor affects placental development. In this study, we investigated the phenotypic characteristics of placentas from Ackr3^-/- embryos to determine how Ackr3 contributes to early placentation. In placentas from Ackr3^-/- embryos, we observed an increase in decidual compa

SUBMITTER: Quinn KE 

PROVIDER: S-EPMC7286785 | biostudies-literature | 2020 Jun

REPOSITORIES: biostudies-literature