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Atypical chemokine receptor 1 on nucleated erythroid cells regulates hematopoiesis.

Abstract：

: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.

journal_name

Nat Immunol

journal_title

Nature immunology

authors

Duchene J,Novitzky-Basso I,Thiriot A,Casanova-Acebes M,Bianchini M,Etheridge SL,Hub E,Nitz K,Artinger K,Eller K,Caamaño J,Rülicke T,Moss P,Megens RTA,von Andrian UH,Hidalgo A,Weber C,Rot A

doi

10.1038/ni.3763

subject

Has Abstract

pub_date

2017-07-01 00:00:00

pages

753-761

issue

7

eissn

1529-2908

issn

1529-2916

pii

ni.3763

journal_volume

18

pub_type

杂志文章

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