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(American Journal of Pathology. 2004;165:1199-1209.)
© 2004 American Society for Investigative Pathology

Impaired Lung Dendritic Cell Activation in CCR2 Knockout Mice

Bo-Chin Chiu*, Christine M. Freeman*, Valerie R. Stolberg{dagger}, Jerry S. Hu*, Kyriaki Zeibecoglou{ddagger}, Bao Lu§, Craig Gerard§, Israel F. Charo, Sergio A. Lira|| and Stephen W. Chensue*{dagger}

From the Department of Pathology,* University of Michigan Medical School, Ann Arbor, Michigan; the Department of Pathology and Laboratory Medicine,{dagger} Veterans Administration Ann Arbor Healthcare System, Ann Arbor, Michigan; NIMTS Veterans Hospital,{ddagger} Athens, Greece; Children’s Hospital,§ Harvard Medical School, Boston, Massachusetts; Gladstone Institute of Cardiovascular Disease, University of California, San Francisco, California; and the Immunobiology Center,|| Mount Sinai School of Medicine, New York, New York

Dendritic cell (DC) recruitment is a hallmark event in antigen (Ag)-challenged lungs. We previously reported models for analyzing DC migration and activation in the lung after Th1- or Th2-eliciting pathogen Ag-bead challenge. To determine the role of chemokines in DC mobilization, we applied this analysis to CCR1, CCR2, CCR5, and CCR6 chemokine receptor knockout mice. Both Mycobacteria bovis protein Ags and helminthic, Schistosoma mansoni egg Ags elicited multiple chemokines, including CCR1, CCR2, CCR5, and to a lesser extent CCR6 ligands. DCs from wild-type lungs expressed transcripts for chemokine receptors, CCR1, CCR2, CCR5, and CXCR4. In all knockout strains, CD11c+ cells were recruited to Ag-beads likely because of receptor redundancy. However, DCs in CCR2–/– mice had significantly decreased MHCII and CD40 expression. This was associated with abrogated cytokine production in draining lymph node cultures. Analysis of local innate inflammation revealed a 50% reduction in macrophage recruitment in CCR2–/– mice. Bone marrow chimeras of mixed CCR2+/+ green fluorescent protein transgenic and CCR2–/– green fluorescent protein-negative cells confirmed the DC maturation defect was only among the latter population. In conclusion, CCR2 knockout confers an intrinsic DC activation defect and CCR2 ligands likely promote the local activation/maturation of inflammatory DCs.




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