Tuberculosis (TB), caused by Mycobacterium tuberculosis (MTB), is a major health problem, with 10 million new cases diagnosed each year. Innate immunity plays an important role in the host defense against M.
tuberculosis, and the first step in this process is recognition of MTB by cells of the innate immune system. Several classes of
pattern recognition receptors (PPRs) are involved in the recognition of M.
tuberculosis, including
Toll-like receptors (TLRs),
C-type lectin receptors (CLRs), and
Nod-like receptors (NLRs). Among the TLR family, TLR2, TLR4, and TLR9 and their adaptor molecule MyD88 play the most prominent roles in the initiation of the immune response against
tuberculosis. In addition to TLRs, other
PRRs such as NOD2,
Dectin-1,
Mannose receptor, and
DC-SIGN are also involved in the recognition of M.
tuberculosis. Human epidemiological studies revealed that genetic variation in genes encoding for
PRRs and downstream signaling products influence
disease susceptibility, severity, and outcome. More insight into
PRRs and the recognition of mycobacteria, combined with immunogenetic studies in TB patients, does not only lead to a better understanding of the pathogenesis of
tuberculosis but also may contribute to the design of novel immunotherapeutic strategies.