Figure 1.

Antimicrobial activity and NOD2-induced autophagy mediate the link between innate and adaptive immunity in mycobacterial infection. The recognition of mycobacterial lipoproteins by the TLR-2/1 heterodimer is a critical way to initiate a pro-inflammatory response and activation of a vitamin-D antimicrobial program against intracellular pathogens such as Mycobacterium leprae. Mycobacterial muramyl dipeptide sensing by NOD2 receptors enhances the inflammatory response in a leucine-rich repeat kinase 2 (LRRK2)-dependent manner and activates autophagic mechanisms. All of these processes lead to mycobacterial killing and are essential for bacterial handling, antigen presentation, and consequent generation of an effective CD4 T cell response.