FIGURE 8.

Macrophage responses during M. tuberculosis infection in the absence (A) or presence (B) of SOCS1. Infection of macrophages with M. tuberculosis induces SOCS1 and secretion of IL-12 in an TLR2/MyD88- and NOD2-mediated manner. SOCS1 probably hampers STAT4 activation and reduces IFN-γ secretion in response to M. tuberculosis-stimulated IL-12. Decreased IFN-γ levels account for diminished levels of activated STAT1 and IFN-regulated effector molecules in the presence of SOCS1. IFN-γ-dependent IL-12Rβ1 expression is also decreased in the presence of SOCS1. As a consequence, higher intracellular mycobacterial levels are observed. Of importance, SOCS1 does not hinder responses to IFN-γ. The secretion of IFN-α/β is also inhibited.