TLR7 Deficiency Leads to TLR8 Compensative Regulation of Immune Response against JEV in Mice

Japanese encephalitis virus (JEV) is a highly fatal pathogen to human beings. Toll-like receptor 7 (TLR7) plays a role as the first host defense against most single-stranded RNA flaviviruses. This study aims to investigate the role of TLR7 in inducing adaptive immune response in mice against JEV. In vitro and in vivo studies were conducted to examine the expression of toll-like receptors (TLRs) in mice. After JEV infection, physical parameters of mice (survival rate and body weight) were evaluated, and organs or cells were collected for further analysis. The expression of TLR7 was increased significantly as compare to other TLR molecules post-JEV infection. The expression of CD80, CD86, and CD273 on bone marrow-derived dendritic cells was increased significantly in TLR7(−/−) mice. Furthermore, viral load was also increased significantly in TLR7(−/−) mice as compare to C57BL/6 mice. But there was no significant difference among survival rate and body weight in TLR7(−/−) mice as compare to C57BL/6. Interestingly, we also found that TLR8 was upregulated in TLR7(−/−) mice. The study concluded that TLR8 was upregulated in TLR7-deficient mice, and it might play a compensatory role in the immune response in TLR7(−/−) mice.