FIG 7.

Role of TREM2 in macrophage antibacterial defense against M. tuberculosis. (A) Entry of M. tuberculosis via TREM2 induces a STING-dependent upregulation of TREM2 expression, which in turn increases IL-10 and IFN-β production. Increased levels of IFN-β is responsible for type I IFN-driven inhibition of ROS production and proinflammatory cytokine production, which results in the increased intracellular survival of M. tuberculosis. (B) Targeting the TREM2 signaling pathway by genetic deletion or antibody-mediated neutralization of TREM2, antibody-mediated neutralization of IFNAR1, or pharmacological inhibition of STING, restores proper proinflammatory cytokine and ROS production to promote bacterial clearance.