Innate immune recognition of Mycobacterium tuberculosis: receptor engagement and inflammatory outcomes at the site of infection

M. tuberculosis is a notorious global pathogen responsible for over a million fatalities annually. It has been estimated that one-third of the world's population is latently infected with M. tuberculosis; however, only ∼10 million individuals develop an active disease annually. The innate immune defence system is the first to encounter the bacilli and initiates a cascade of events to protect the host from developing tuberculosis. Innate immune cells such as pulmonary epithelial cells, alveolar macrophages, and dendritic cells express Toll-like Receptors (TLRs), C-type Lectin Receptors (CLRs), NOD-like Receptors (NLRs), Scavenger Receptors, Surfactant Proteins, RIG-I–like Receptors (RLRs), Complement Receptors, and Fc Receptors upon exposure to M. tuberculosis Pathogen-Associated Molecular Patterns (PAMPs). The interaction between host Pathogen Recognition Receptors (PRRs) and M. tuberculosis PAMPs results in the activation of several signalling pathways that initiate an inflammatory response through the production of cytokines and chemokines at the site of infection. This Surface Feature manuscript provides an up-to-date report on the expression of host PRRs in pulmonary epithelial cells, alveolar macrophages and dendritic cells and their interactions with M. tuberculosis PAMPs to initiate an inflammatory response at the site of infection. Furthermore, this manuscript sheds light on the role of this inflammatory response as a “double-edged sword” in the fight against M. tuberculosis infection. Understanding these interactions provides a directive for host-directed therapies to modulate the innate immune response.