Table 2.

Examples of Mtb immune evasion strategies discussed at the workshop.

Host defense strategies	Mycobacterial counterstrategies^a
Recruit microbicidal macrophages to site of infection	Mask PAMPS with cell surface lipids to avoid recruitment of TLR-signaled microbicidal macrophages Recruit growth-permissive macrophages through induction of the monocyte chemokine CCL2
Promote phagosome – lysosome fusion	Avoid and/or tolerate Mtb phagosome-microbicidal lysosome fusion
Aggregate macrophages into epithelioid granulomas to restrict and contain mycobacteria	Use early granuloma for intracellular expansion through macrophage-to-macrophage spread Activate granuloma-specific genes that may help mycobacteria to survive in the granuloma Vascularize the granuloma to make it conducive to bacterial growth
Processing and presentation of bacterial Ags	Inhibit MHC-II Ag processing and presentation Divert secreted Ags from the MHC class II pathway to the export pathway, to avoid CD4 T cell recognition Alter Ag expression to evade T cell recognition by inducing suboptimal activation of CD4 effector cells Avoid focusing T cell immune responses to conserved and/or subdominant regions
Activation of T cells to control infection	Release PAMPs to inhibit TCR signaling and induce CD4 + T cell anergy Delay DC migration to lymph nodes in order to delay generation of effector T cells
Increase microbicidal capacity of the granuloma by recruiting effector T cells to it	Induce antigen-specific Treg cells that delay effector T cell priming, and recruitment to granuloma Downregulate key mycobacterial antigens so as to render infected macrophages “invisible” to pathogen-specific effector T cells Induce suppressive factors (e.g., NO, IL-10, and TGFb) that restrict effector T cell function

[4,62–64].