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• W2620512953 abstract "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." @default.
• W2620512953 created "2017-06-05" @default.
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• W2620512953 date "2017-05-29" @default.
• W2620512953 modified "2023-10-17" @default.
• W2620512953 title "Atypical chemokine receptor 1 on nucleated erythroid cells regulates hematopoiesis" @default.
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• W2620512953 doi "https://doi.org/10.1038/ni.3763" @default.
• W2620512953 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5480598" @default.
• W2620512953 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/28553950" @default.
• W2620512953 hasPublicationYear "2017" @default.
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