Regulation of type I interferon factor secretion via the TLR3 signaling pathway after PRV infection of mouse trigeminal ganglion cells.

This study investigates the effects of pseudorabies virus (PRV) infection on the antiviral immune signaling pathway and type I interferon factors in mouse trigeminal ganglion (TG) cells. The experiment involved inoculating TG primary cells with PRV and intranasally infecting mice. The results indicated that PRV infection of mouse TG primary cells led to alterations in the gene and protein expression of TLR3, TRIF, TBK1, and IRF3, while inhibiting the expression of IκBα protein in the later stages of infection. Additionally, the phosphorylation of IRF3 and IκBα was induced both in vivo and in vitro. Following PRV infection, the expression of IFN-α was up-regulated in the supernatant, whereas its expression was down-regulated in the cell lysates and mouse TG. To further investigate the role of TLR3 in the IRF3 signaling pathway and type I interferon factors, siRNA was employed to interfere with TLR3 expression in TG cells. Western blot analysis was conducted to assess the expression of TLR3 signaling pathway-related proteins and the secretion of IFN-α following the interference. The findings demonstrated that siTLR3 effectively reduced TLR3 protein expression in TG cells and concurrently modulated the secretion of type I interferon factors via the TLR3-TRIF-TBK1-IRF3 signaling axis. Furthermore, PRV infection was shown to induce TLR3 expression in both mouse TG primary cells and mouse TG, thereby activating the TLR3-TRIF-TBK1-IRF3 signaling axis to regulate the antiviral immune response in TG cells, while simultaneously inhibiting IFN-α expression within TG cells and TG through the TLR3 signaling pathway. These experimental results elucidate the antiviral immune mechanism associated with the TLR3 signaling pathway following PRV infection of mouse TG cells, offering new insights into the immune evasion strategies employed by PRV.