| First Author | Quinn KE | Year | 2020 |
| Journal | Placenta | Volume | 95 |
| Pages | 18-25 | PubMed ID | 32452398 |
| Mgi Jnum | J:318909 | Mgi Id | MGI:6863734 |
| Doi | 10.1016/j.placenta.2020.04.007 | Citation | Quinn KE, et al. (2020) Deletion of atypical chemokine receptor 3 (ACKR3) increases immune cells at the fetal-maternal interface. Placenta 95:18-25 |
| abstractText | 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 compaction and in the size of the uterine natural killer cell population. Ackr3 knockdown in trophoblast cells led to a decrease in trophoblast migration. These findings suggest that this decoy receptor may therefore be an important factor in normal placentation. |
