Basic mechanisms of lipid droplet biogenesis in macrophages infected with M. leprae. TLR mediated uptake of M. leprae: M. leprae attaches to TLR2 and TLR6. Heterodimerization of TLR2 and TLR6 induces downstream signalling and subsequent cholesterol accumulation by LDs formation [32, 33]. In SCs, TLR6, but not TLR2, is essential for M. leprae-induced LDs biogenesis [5]. Cholesterol accumulates at the site of mycobacterial entry and promotes mycobacterial uptake. Cholesterol also recruits TACO from the plasma membrane to the phagosome [34]. TACO prevents phagosome-lysosome fusion and promotes intracellular survival [35, 36]. Uptake by scavenger receptors (proven for M. tuberculosis, hypothetical for M. leprae): reactive oxygen species might oxidize low-density lipoprotein (LDL) to oxLDL, which is thought to be subsequently bound and taken up by scavenger receptors CD36 and LOX1. A: ADRP; CHO: cholesterol; P: perilipin. Unknown mechanisms for LDs induction are indicated with a question mark.
