We previously demonstrated the activation of the antigen-presenting function in cochlear macrophages after acoustic injury,7 which is consistent with a previous study of the induction of MHC II expression following immune challenge by sterile labyrinthitis in the cochlea.34 Here, we demonstrated that the lack of Tlr4 function suppresses the noise-induced production of MHC II, suggesting that Tlr4 participates in noise-induced antigen-presentation activity. Here, TLR4 is linked to inner ear disorder.