Figure 7

Figure 7

Model for the impact of negative regulator NLR nlrc3-like on innate immune responses during mycobacterial infection. During the early stage of infection, the defect of nlrc3-like can boost the expression of mycobacterial elicited pro-inflammatory genes via Asc mediated inflammasome activation in infected macrophages, which results in a bacterial killing effect accompanied by an increased neutrophil recruitment. However, during the late stage of infection the host shifts into a hyperinflammatory status with uncontrolled excessive neutrophil infiltration and increased tissue damage and death. The administration of DEX can block the excessive inflammatory response and improve disease outcome.