Toll-Like Receptor Adaptor Molecules Enhance DNA-Raised Adaptive Immune Responses against Influenza and Tumors through Activation of Innate Immunity

摘要: Toll-like receptors (TLRs) recognize microbial components and trigger the signaling cascade that activates innate adaptive immunity. TLR adaptor molecules play a central role in this cascade; thus, we hypothesized overexpression of could mimic infection without any components. Dual-promoter plasmids carry an antigen molecule such as Toll-interleukin-1 receptor domain-containing adaptor-inducing beta interferon (TRIF) or myeloid differentiation factor 88 (MyD88) were constructed administered to mice determine if these can act adjuvant. A DNA vaccine incorporated with MyD88 genetic adjuvant enhanced antigen-specific humoral immune responses, whereas TRIF cellular responses. Incorporating targeting influenza HA tumor-associated E7 conferred superior protection. These results indicate bridge immunity potentiate effects vaccines against virus tumors.