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ChemR23, a putative chemoattractant receptor, is expressed in monocyte‐derived dendritic cells and macrophages and is a coreceptor for SIV and some primary HIV‐1 strains

ChemR23, a putative chemoattractant receptor, is expressed in monocyte‐derived dendritic cells... Leukocyte chemoattractants act through a rapidly growing subfamily of G protein‐coupled receptors. We report the cloning of a novel human gene encoding an orphan receptor (ChemR23) related to the C3a, C5a and formyl Met‐Leu‐Phe receptors, and more distantly to the subfamilies of chemokine receptors. ChemR23 transcripts were found to be abundant in monocyte‐derived dendritic cells and macrophages, treated or not with LPS. Low expression could also be detected by reverse transcription‐PCR in CD4+ T lymphocytes. The gene encoding ChemR23 was assigned by radiation hybrid mapping to the q21.2 – 21.3 region of human chromosome 12, outside the gene clusters identified so far for chemoattractant receptors. Given the increasing number of chemoattractant receptors used by HIV‐1, HIV‐2 and SIV as coreceptors, ChemR23 was tested in fusion assays for potential coreceptor activity by a range of viral strains. None of the tested HIV‐2 strains made use of ChemR23 as a coreceptor, but several SIV strains (SIVmac316, SIVmac239, SIVmac17E‐Fr and SIVsm62A), as well as a primary HIV‐1 strain (92UG024‐2) used it efficiently. ChemR23 therefore appears as a coreceptor for immunodeficiency viruses that does not belong to the chemokine receptor family. It is also a putative chemoattractant receptor relatively specific for antigen‐presenting cells, and it could play an important role in the recruitment or trafficking of these cell populations. Future work will be required to identify the ligand(s) of this new G protein‐coupled receptor and to define its precise role in the physiology of dendritic cells and macrophages. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png European Journal of Immunology Wiley

ChemR23, a putative chemoattractant receptor, is expressed in monocyte‐derived dendritic cells and macrophages and is a coreceptor for SIV and some primary HIV‐1 strains

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References (63)

Publisher
Wiley
Copyright
© 1998 WILEY‐VCH Verlag GmbH, Weinheim, Fed. Rep. of Germany
ISSN
0014-2980
eISSN
1521-4141
DOI
10.1002/(SICI)1521-4141(199805)28:05<1689::AID-IMMU1689>3.0.CO;2-I
pmid
9603476
Publisher site
See Article on Publisher Site

Abstract

Leukocyte chemoattractants act through a rapidly growing subfamily of G protein‐coupled receptors. We report the cloning of a novel human gene encoding an orphan receptor (ChemR23) related to the C3a, C5a and formyl Met‐Leu‐Phe receptors, and more distantly to the subfamilies of chemokine receptors. ChemR23 transcripts were found to be abundant in monocyte‐derived dendritic cells and macrophages, treated or not with LPS. Low expression could also be detected by reverse transcription‐PCR in CD4+ T lymphocytes. The gene encoding ChemR23 was assigned by radiation hybrid mapping to the q21.2 – 21.3 region of human chromosome 12, outside the gene clusters identified so far for chemoattractant receptors. Given the increasing number of chemoattractant receptors used by HIV‐1, HIV‐2 and SIV as coreceptors, ChemR23 was tested in fusion assays for potential coreceptor activity by a range of viral strains. None of the tested HIV‐2 strains made use of ChemR23 as a coreceptor, but several SIV strains (SIVmac316, SIVmac239, SIVmac17E‐Fr and SIVsm62A), as well as a primary HIV‐1 strain (92UG024‐2) used it efficiently. ChemR23 therefore appears as a coreceptor for immunodeficiency viruses that does not belong to the chemokine receptor family. It is also a putative chemoattractant receptor relatively specific for antigen‐presenting cells, and it could play an important role in the recruitment or trafficking of these cell populations. Future work will be required to identify the ligand(s) of this new G protein‐coupled receptor and to define its precise role in the physiology of dendritic cells and macrophages.

Journal

European Journal of ImmunologyWiley

Published: May 1, 1998

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