Figure 4.

Schematic representation of the potential effects of the naturally occurring inhibitors of TGF-β, decorin and LAP, on TGF-β activity in situ. Presumably at sites of active MTB infection, such as tuberculous granulomas, TGF-β is produced by the mononuclear phagocytes (Mφ), which are infected with MTB and/or exposed to MTB antigens. Through positive autoregulation initiated by TGF-β itself (+), high tissue levels of the cytokine are maintained. Excess TGF-β undermines antimycobacterial defenses by suppression of T cell function and deactivation of macrophages. Decorin and LAP counteract (straight arrows) the effects of TGF-β and thereby interrupt both autoinduction and immunosuppression.