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Mycobacterium tuberculosis (Mtb) is the causative agent of tuberculosis (TB) which causes the death of over 1.5 million people per year [1]. Despite the availability of multiple anti-TB drugs and a vaccine (Mycobacterium bovis bacillus Calmette–Guérin (BCG)), Mtb is still a common cause of morbidity for a large fraction of the human population. Despite having been administered to more than 3.5 billion people since its development in the early twentieth century, BCG confers highly variable protection. In vaccinated infants, it is able to provide significant protection against severe forms of TB, especially disseminating and meningeal forms but its efficacy against adult pulmonary is inconsistent and incomplete. Therefore for a better control of TB, a better vaccine is needed that is able to confer lifelong protection.

Macrophages and dendritic cells (DCs) have an important role in orchestrating both the innate and adaptive immunity against Mycobacteria. After the bacteria have been recognized by these cells through the engagement of various pathogen recognition receptors (PRRs) such as the toll-like receptors (TLRs), C-type lectin receptors (CLRs) and Nod-like receptors (NLRs), host innate responses are initiated which finally results in the activation of adaptive immunity, primarily T cell responses. CLRs have been implicated in the phagocytosis of the bacterium but phagocytosis alone does not lead to immune activation [2-4]. The TLRs implicated in the initiation of immune responses against Mycobacterium are TLR2, TLR4 TLR9 and possibly TLR8 [5]. TLR9 recognizes unmethylated CpG motifs with mycobacterium DNA, whereas TLR2 has many …