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,#
,¶
* Gladstone Institute of Cardiovascular Disease, San Francisco, CA 94141;
Howard Hughes Medical Institute, Department of Microbiology and Immunology,
Biomedical Science Graduate Program,
Cardiovascular Research Institute, Department of Medicine, and
¶ Daiichi Research Center, University of California, San Francisco, CA 94143;
|| Department of Internal Medicine, Ludwig-Maximilians University, Munich, Germany; and
# Departments of Medicine and Microbiology, New York University School of Medicine, New York, NY 10016
We previously reported that CCR2–/– mice are susceptible to Mycobacterium tuberculosis infection. Susceptibility was associated with an early and sustained macrophage trafficking defect, followed by delayed recruitment of dendritic cells (DCs) and T cells to the lungs. However, the relative importance of the lack of CCR2 expression by macrophages and DCs vs T cells in susceptibility to infection was unclear. In this study, we used mixed bone marrow transplantation to create mice in which the genotype of the T cells was either CCR2+/+ or CCR2–/– while maintaining the genotype of the myeloid cells as CCR2+/+. After infection with M. tuberculosis, we found that the genotype of the macrophages and/or DCs, but not that of the T cells, was critical for both T cell and myeloid cell migration to the lungs. Further investigation revealed a critical role for CCR2 in the recruitment of F4/80dim macrophages and CD11cdim/intermediate DCs to the infected lung.
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