In vivo, infecting TLR3 KO mice with CVB3 confirmed these data, as DCs from the spleen and mediastinal lymph nodes presented an inhibitory phenotype compared to WT cells, we speculate that viral dsRNA formed after CVB3 replication is recognized by TLR3 and, through TRIF signaling, results in changes on expression of antigen-presenting molecules, although we cannot exclude the possibilities that CVB3 differently infect TLR3 KO DCs and that infection of the host may also indirectly affect the functions of DCs. This evidence concerns the gene TLR3 and infection.