Mycobacterium tuberculosis expresses molecular motifs that are potent TLR agonists,
targeting especially TLR2, and resulting in rapid activation of cells of the innate immune system. The
control of experimental acute M. tuberculosis infection seems rather independent of the presence of
TLRs, as is the induction of adaptive immunity to mycobacteria, while long term control of chronic
infection might be more TLR dependent. Conversely, some molecules produced by M. tuberculosis can
modulate the host innate TLR mediated responses. Control of M. tuberculosis infection depends on a
balance between the host recognition of the pathogen and activation of both innate and adaptive
immune responses, and immune evasion strategies developed by the bacteria.
Keywords: TLRs, tuberculosis, mycobacterial cell wall, PAMPS, macrophages, dendritic cells.