Researchers have found out the mechanism1 behind a clever tactic used by pathogenic mycobacteria to evade immune surveillance and survive in host macrophages. The knowledge could help create better therapeutic tools to tackle mycobacterium infection.
Mycobacteria are known to downregulate the expression of class II transactivator (CIITA)/MHC-II thereby affecting antigen presentation.
However, the precise role for specific signaling components executing down-regulation of CIITA/MHC-II had not been studied yet. The researchers showed with Mycobacterium bovis bacillus how a signalling function supresses the function of this class II transactivator.
Technically speaking, they found how a Calmette-Guérin (BCG)-mediated TLR2 signaling-induced iNOS/NO expression and how this in turn helped suppress the IFN-γ-induced CIITA/MHC-II functions.
The study shows the novel role of this process in dictating the mycobacterial capacity to inhibit CIITA/MHC-II-mediated antigen presentation by infected macrophages. This helps the mycobacteria elude immune surveillance. The study is promising for new therapeutic protocols that could look at breaking this evasion mechanism.
