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Am J Pathol. 2004 Jan;164(1):49-57.

Toll-like receptor 2-deficient mice succumb to Mycobacterium tuberculosis infection.

Author information

1
Department of Immunology, Groote Schuur Hospital, University of Cape Town, Cape Town, South Africa. mdrennan@uctgsh1.uct.ac.za

Abstract

Recognition of Mycobacterium tuberculosis by the innate immune system is essential in the development of an adaptive immune response. Mycobacterial cell wall components activate macrophages through Toll-like receptor (TLR) 2, suggesting that this innate immune receptor plays a role in the host response to M. tuberculosis infection. After aerosol infection with either 100 or 500 live mycobacteria, TLR2-deficient mice display reduced bacterial clearance, a defective granulomatous response, and develop chronic pneumonia. Analysis of pulmonary immune responses in TLR2-deficient mice after 500 mycobacterial aerosol challenge showed increased levels of interferon-gamma, tumor necrosis factor-alpha, and interleukin-12p40 as well as increased numbers of CD4(+) and CD8(+) cells. Furthermore, TLR2-deficient mice mounted elevated Ag-specific type 1 T-cell responses that were not protective because all deficient mice succumb to infection within 5 months. Taken together, the data suggests that TLR2 may function as a regulator of inflammation, and in its absence an exaggerated immune inflammatory response develops.

PMID:
14695318
PMCID:
PMC1602241
DOI:
10.1016/S0002-9440(10)63095-7
[Indexed for MEDLINE]
Free PMC Article

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