Chemokine receptor 2 serves an early and essential role in resistance to Mycobacterium tuberculosis.

Peters W, Scott HM, Chambers HF, Flynn JL, Charo IF, Ernst JD
Proc Natl Acad Sci U S A. 2001 98 (14): 7958-63

PMID: 11438742 · PMCID: PMC35450 · DOI:10.1073/pnas.131207398

Although the protective cellular immune response to Mycobacterium tuberculosis requires recruitment of macrophages and T lymphocytes to the site of infection, the signals that regulate this trafficking have not been defined. We investigated the role of C-C chemokine receptor 2 (CCR2)-dependent cell recruitment in the protective response to M. tuberculosis. CCR2(-/-) mice died early after infection and had 100-fold more bacteria in their lungs than did CCR2(+/+) mice. CCR2(-/-) mice exhibited an early defect in macrophage recruitment to the lung and a later defect in recruitment of dendritic cells and T cells to the lung. CCR2(-/-) mice also had fewer macrophages and dendritic cells recruited to the mediastinal lymph node (MLN) after infection. T cell migration through the MLN was similar in CCR2(-/-) and CCR2(+/+) mice. However, T cell priming was delayed in the MLNs of the CCR2(-/-) mice, and fewer CD4(+) and CD8(+) T cells primed to produce IFN-gamma accumulated in the lungs of the CCR2(-/-) mice. These data demonstrate that cellular responses mediated by activation of CCR2 are essential in the initial immune response and control of infection with M. tuberculosis.

MeSH Terms (9)

Animals Cell Movement Immunity, Innate Mice Mycobacterium tuberculosis Receptors, CCR2 Receptors, Chemokine T-Lymphocytes Tuberculosis

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