Asset Details
Do you wish to reserve the book?
Atypical chemokine receptor 1 on nucleated erythroid cells regulates hematopoiesis
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Atypical chemokine receptor 1 on nucleated erythroid cells regulates hematopoiesis
Do you wish to request the book?
Atypical chemokine receptor 1 on nucleated erythroid cells regulates hematopoiesis
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Atypical chemokine receptor 1 on nucleated erythroid cells regulates hematopoiesis
2017
Overview
Genetic polymorphisms affect expression of the atypical chemokine receptor ACKR1 (Duffy) on nucleated erythrocyte precursors. Rot and colleagues show that loss of its expression alters hematopoiesis, yielding a distinct neutrophil population that rapidly exits the bloodstream to give an apparent ‘neutropenia’ phenotype.
Healthy individuals of African ancestry have neutropenia that has been linked with the variant rs2814778(G) of the gene encoding atypical chemokine receptor 1 (
ACKR1
). This polymorphism selectively abolishes the expression of ACKR1 in erythroid cells, causing a Duffy-negative phenotype. Here we describe an unexpected fundamental role for ACKR1 in hematopoiesis and provide the mechanism that links its absence with neutropenia. Nucleated erythroid cells had high expression of ACKR1, which facilitated their direct contact with hematopoietic stem cells. The absence of erythroid ACKR1 altered mouse hematopoiesis including stem and progenitor cells, which ultimately gave rise to phenotypically distinct neutrophils that readily left the circulation, causing neutropenia. Individuals with a Duffy-negative phenotype developed a distinct profile of neutrophil effector molecules that closely reflected the one observed in the ACKR1-deficient mice. Thus, alternative physiological patterns of hematopoiesis and bone marrow cell outputs depend on the expression of ACKR1 in the erythroid lineage, findings with major implications for the selection advantages that have resulted in the paramount fixation of the
ACKR1
rs2814778(G) polymorphism in Africa.
Publisher
Nature Publishing Group US,Nature Publishing Group
Subject
/ 13/51
/ 14/105
/ 14/19
/ 14/69
/ 38
/ 59
/ Animals
/ Biomedical and Life Sciences
/ Bone Marrow Cells - metabolism
/ Duffy Blood-Group System - genetics
/ Duffy Blood-Group System - metabolism
/ Fluorescent Antibody Technique
/ Hematopoietic Stem Cells - cytology
/ Hematopoietic Stem Cells - metabolism
/ Humans
/ Mice
/ Receptors, Cell Surface - genetics
/ Receptors, Cell Surface - metabolism
/ Receptors, Chemokine - genetics
/ Receptors, Chemokine - metabolism
/ Rodents
