Blood · 2017
The atypical receptor CCRL2 is required for CXCR2-dependent neutrophil recruitment and tissue damage.
СтатьяНазвание и аннотация: Перевод в очереди
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Del Prete Annalisa, Martínez-Muñoz Laura, Mazzon Cristina, Toffali Lara, Sozio Francesca, Za Lorena, Bosisio Daniela, Gazzurelli Luisa, Salvi Valentina, Tiberio Laura, Liberati Chiara, Scanziani Eugenio, Vecchi Annunciata, Laudanna Carlo, Mellado Mario, Mantovani Alberto, Sozzani Silvano
Аннотация
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.