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- ,
tumor necrosis factor- , 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
