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Innate immunity against Mycobacterium tuberculosis is a critical early response to prevent the establishment of the infection. Despite recent advances in understanding the host-pathogen dialogue in the early stages of tuberculosis (TB), much has yet to be learnt. The nature and consequences of this dialogue ultimately determine the path of infection: namely, either early clearance of M. tuberculosis, or establishment of M. tuberculosis infection leading to active TB disease and/or latent TB infection. On the frontline in innate immunity are pattern recognition receptors (PRRs), with soluble factors (e.g. collectins and complement) and cell surface factors (e.g. Toll-like receptors and other C-type lectin receptors (Dectin 1/2, Nod-like receptors, DC-SIGN, Mincle, mannose receptor, and MCL) that play a central role in recognising M. tuberculosis and facilitating its clearance. However, in a 'double-edged sword' scenario, these factors can also be involved in enhancement of pathogenesis as well. Furthermore, innate immunity is also a critical bridge in establishing the subsequent adaptive immune response, which is also responsible for granuloma formation that cordons off M. tuberculosis infection, establishing latency and acting as a reservoir for bacterial persistence and dissemination of future disease. This chapter discusses the current understanding of pattern recognition of M. tuberculosis by innate immunity and the role this plays in the pathogenesis and protection against TB. |
