+1 Recommend
0 collections
      • Record: found
      • Abstract: found
      • Article: not found

      Chemokine receptor CCR2 but not CCR5 or CCR6 mediates the increase in pulmonary dendritic cells during allergic airway inflammation.

      The Journal of Immunology Author Choice

      physiology, Animals, Apoptosis, Asthma, immunology, Cell Movement, Dendritic Cells, Lung, Mice, Mice, Inbred C57BL, Monocytes, Receptors, CCR2, Receptors, CCR5, Receptors, CCR6, Receptors, Chemokine

      Read this article at

          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.


          Increased numbers of pulmonary dendritic cells (DCs) are recruited to the lungs during allergic airway inflammation and contribute to the maintenance of the inflammatory immune response. The chemokine receptors that directly control DC accumulation into the lungs are largely unknown. To explore this issue, we generated mixed bone marrow chimeric mice containing both wild-type and knockout cells for a given chemokine receptor. After induction of allergic airway inflammation, we specifically tracked and compared chemokine receptor knockout vs wild-type DC populations through various lung compartments. Using this approach, we show that CCR2, but not CCR5 or CCR6, directly controls the accumulation of DCs into allergic lungs. Furthermore, the size of inflammatory monocyte populations in peripheral blood was strikingly CCR2 dependent, suggesting that CCR2 primarily mediates the release of monocytic DC precursors into the bloodstream.

          Related collections

          Author and article information



          Comment on this article