Nonredundant role of CCRL2 in lung dendritic cell trafficking

Karel Otero, Annunciata Vecchi, Emilio Hirsch, Jennifer Kearley, William Vermi, Annalisa Del Prete, Safiyè Gonzalvo-Feo, Cecilia Garlanda, Ornella Azzolino, Laura Salogni, Clare M. Lloyd, Fabio Facchetti, Alberto Mantovani, Silvano Sozzani

Research output: Contribution to journalArticlepeer-review


Chemokine CC motif receptor-like 2 (CCRL2) is a heptahelic transmembrane receptor that shows the highest degree of homology with CCR1, an inflammatory chemokine receptor. CCRL2 mRNA was rapidly (30 minutes) and transiently (2-4 hours) regulated during dendritic cell (DC) maturation. Protein expression paralleled RNA regulation. In vivo, CCRL2 was expressed by activated DC and macrophages, but not by eosinophils and T cells. CCRL2-/- mice showed normal recruitment of circulating DC into the lung, but a defective trafficking of antigen-loaded lung DC to mediastinal lymph nodes. This defect was associated to a reduction in lymph node cellularity and reduced priming of T helper cell 2 response. CCRL2-/- mice were protected in a model of ovalbumin-induced airway inflammation, with reduced leukocyte recruitment in the BAL (eosinophils and mononuclear cells) and reduced production of the T helper cell 2 cytokines, interleukin-4 and -5, and chemokines CCL11 and CCL17. The central role of CCRL2 deficiency in DC was supported by the fact that adoptive transfer of CCRL2-/- antigen-loaded DC in wild-type animals recapitulated the phenotype observed in knockout mice. These data show a nonredundant role of CCRL2 in lung DC trafficking and propose a role for this receptor in the control of excessive airway inflammatory responses.

Original languageEnglish
Pages (from-to)2942-2949
Number of pages8
Issue number16
Publication statusPublished - Oct 21 2010

ASJC Scopus subject areas

  • Hematology
  • Biochemistry
  • Cell Biology
  • Immunology


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