Research Paper Volume 13, Issue 1 pp 1440—1457

NLRC4 gene silencing-dependent blockade of NOD-like receptor pathway inhibits inflammation, reduces proliferation and increases apoptosis of dendritic cells in mice with septic shock

NLRC4 gene regulates inflammatory reaction and immune response of DCs in septic shock by mediating the NLR pathway.NLRC4 is the receptor of the NLR pathway. Activated NF-κB pathway induces inflammatory reaction with secretion of inflammatory factors: IL-1β, TNF-α and IL-6 outside cells, as well as increases in CD80, CD86 and MHC II on the cytomembrane, thus activating DC immune response. Importantly, siRNA-mediated silencing of NLRC4 blocks the NLR signaling pathway to inhibit DC maturation and immune response, which alleviates the lung tissue injury of mice induced by septic shock.

Figure 7. NLRC4 gene regulates inflammatory reaction and immune response of DCs in septic shock by mediating the NLR pathway.NLRC4 is the receptor of the NLR pathway. Activated NF-κB pathway induces inflammatory reaction with secretion of inflammatory factors: IL-1β, TNF-α and IL-6 outside cells, as well as increases in CD80, CD86 and MHC II on the cytomembrane, thus activating DC immune response. Importantly, siRNA-mediated silencing of NLRC4 blocks the NLR signaling pathway to inhibit DC maturation and immune response, which alleviates the lung tissue injury of mice induced by septic shock.