FIG 1.

M. tuberculosis inhibits effective antigen presentation. (A) Schematic of a normal response to phagocytosed bacteria. Antigen-presenting cells phagocytose a pathogen. Fusion of the phagolysosome causes degradation and production of pathogen-specific peptides. Pathogen-derived peptides then bind to the MHC-II complex and are trafficked to the surface of the cell. There, T cells recognize the presented antigen leading to increased immune cell recruitment, cytokine production, and antibody memory. (B) A schematic of M. tuberculosis (Mtb)-mediated evasion of antigen presentation. The APC engulfs M. tuberculosis, and the expression of PE_PGRS47 and EsxG-EsxH inhibits phagolysosome fusion by preventing the degradation of M. tuberculosis antigens. Innate immune detection of lipoproteins results in the activation of TLR2 by M. tuberculosis, which inhibits the induction of CIITA and MHC-II through unknown mechanisms. Together, these M. tuberculosis-mediated alterations prevent the effective expression of MHC molecules and prevents effective clearance by M. tuberculosis-specific T cells.