FIG. 1.

M. tuberculosis-derived glycolipids promote survival in the host Mφ and evasion of the host immune response. M. tuberculosis (MTB) resident in the host Mφ phagosome sheds PIM and LAM to exert effects on intracellular vesicle trafficking. LAM prevents trafficking of late endosomes (LE) to the phagosome, thus inhibiting delivery of Ag presentation machinery and inhibiting the adaptive immune response (21, 22). Although not directly proven, evasion of innate immune responses might be similarly mediated, via inhibition of primary and secondary granule trafficking. PIM enhances delivery of early and recycling endosomes (EE) to the phagosome and is suggested to increase levels of essential nutrients in the phagosome, thus contributing to M. tuberculosis survival (79). Tf, transferrin.