The atypical receptor CCRL2 is required for CXCR2-dependent neutrophil recruitment and tissue damage.
Blood
; 130(10): 1223-1234, 2017 09 07.
Article
em En
| MEDLINE
| ID: mdl-28743719
ABSTRACT
CCRL2 is a 7-transmembrane domain receptor that shares structural and functional similarities with the family of atypical chemokine receptors (ACKRs). CCRL2 is upregulated by inflammatory signals and, unlike other ACKRs, it is not a chemoattractant-scavenging receptor, does not activate ß-arrestins, and is widely expressed by many leukocyte subsets. Therefore, the biological role of CCRL2 in immunity is still unclear. We report that CCRL2-deficient mice have a defect in neutrophil recruitment and are protected in 2 models of inflammatory arthritis. In vitro, CCRL2 was found to constitutively form homodimers and heterodimers with CXCR2, a main neutrophil chemotactic receptor. By heterodimerization, CCRL2 could regulate membrane expression and promote CXCR2 functions, including the activation of ß2-integrins. Therefore, upregulation of CCRL2 observed under inflammatory conditions is functional to finely tune CXCR2-mediated neutrophil recruitment at sites of inflammation.
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Artrite
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Receptores de Quimiocinas
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Receptores de Interleucina-8B
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Neutrófilos
Limite:
Animals
Idioma:
En
Ano de publicação:
2017
Tipo de documento:
Article