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Immunology. 2003 Aug;109(4):547-51.

Role of chemokine ligand 2 in the protective response to early murine pulmonary tuberculosis.

Author information

1
Department of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins, Colorado 80523, USA.

Abstract

Chemokines play an important role in the development of immunity to tuberculosis. Chemokine ligand 2 (CCL2, JE, monocyte chemoattractant protein-1) is thought to be primarily responsible for recruiting monocytes, dendritic cells, natural killer cells and activated T cells, all of which play critical roles in the effective control of tuberculosis infection in mice. We show here that in mice in which the CCL2 gene was disrupted, low-dose aerosol infection with Mycobacterium tuberculosis resulted in fewer macrophages entering the lungs, but only a minor and transient increase in bacterial load in the lungs; these mice were still able to establish a state of chronic disease. Such animals showed similar numbers of activated T cells as wild-type mice, as determined by their expression of the CD44hi CD62lo phenotype, but a transient reduction in cells secreting interferon-gamma. These data indicate that the primary deficiency in mice unable to produce CCL2 is a transient failure to focus antigen-specific T lymphocytes into the infected lung, whereas other elements of the acquired host response are compensated for by different ligands interacting with the chemokine receptor CCR2.

PMID:
12871221
PMCID:
PMC1783002
DOI:
10.1046/j.1365-2567.2003.01680.x
[Indexed for MEDLINE]
Free PMC Article

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