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. 2017 Sep 7;130(10):1223-1234.
doi: 10.1182/blood-2017-04-777680. Epub 2017 Jul 25.

The Atypical Receptor CCRL2 Is Required for CXCR2-dependent Neutrophil Recruitment and Tissue Damage

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The Atypical Receptor CCRL2 Is Required for CXCR2-dependent Neutrophil Recruitment and Tissue Damage

Annalisa Del Prete et al. Blood. .
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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 β-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 β2-integrins. Therefore, upregulation of CCRL2 observed under inflammatory conditions is functional to finely tune CXCR2-mediated neutrophil recruitment at sites of inflammation.

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