Conclusions
Recent studies demonstrate that TLR2 and TLR4 mediate
several macrophage responses to M. tuberculosis and prompt
numerous new questions. Are other TLRs involved in
macrophage responses to M. tuberculosis? What are the components
of M. tuberculosis, in addition to 19 kDa and 38 kDa
lipoproteins, that interact with TLRs and do these components
affect virulence? Does persistent activation of one or
more TLR account for the prolonged inflammatory
response to M. tuberculosis? Are there polymorphisms in the
genes encoding TLRs or proteins downstream of them that
account for variable human susceptibility to tuberculosis?
Research on TLR–mycobacteria interactions will provide
important information regarding the initiation of the host
response to infection, as well as suggest candidates for inclusion
in vaccines.