The atypical receptor CCRL2 is required for CXCR2-dependent neutrophil recruitment and tissue damage

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.

Source: Blood - September 7, 2017 Category: Hematology Authors: Del Prete, A., Martinez-Munoz, L., Mazzon, C., Toffali, L., Sozio, F., Za, L., Bosisio, D., Gazzurelli, L., Salvi, V., Tiberio, L., Liberati, C., Scanziani, E., Vecchi, A., Laudanna, C., Mellado, M., Mantovani, A., Sozzani, S. Tags: Immunobiology and Immunotherapy, Phagocytes, Granulocytes, and Myelopoiesis Source Type: research