Leukocyte migration is a very tightly regulated process involved in homeostatic and pathological conditions with chemokines being the master regulators of this dynamic process. Chemokines control leukocyte trafficking through the interaction with their cognate receptors, belonging to the family of G protein-coupled seven transmembrane surface proteins. A subset of proteins highly homologous to conventional chemokine receptors but unable to activate signal transduction through G proteins, named Atypical Chemokine Receptors (ACKRs), has been characterized to play a crucial role in the negative control of inflammation. CCRL2 is a seven-transmembrane receptor, which shares structural features with ACKRs. However, CCRL2 does not bind chemokines and is devoid of scavenging functions. The only commonly recognized CCRL2 ligand is chemerin, a non-chemokine chemotactic protein. CCRL2 is expressed both by leukocytes and non-hematopoietic cells. The genetic ablation of CCRL2 has been instrumental to elucidate the role of this receptor in different pathological conditions, in particular in inflammatory diseases and cancer.
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(January 1, 2013 - )