Autoimmune sensorineural hearing loss (ASNHL) is diagnosed by excluding ototoxicity, systemic immunologic disease, infections or tumors, and by a therapeutic response to corticosteroids. The relative prominence of B or T cells in ASNHL remains controversial.

We tested our hypothesis that Th1-like effector T cells have a pivotal role in ASNHL in an inner ear-specific mouse model system. We searched for immunogenic peptides within inner ear proteins using our binding motif for IA^s and IA^q MHC class II molecules. ELISA was used to characterize the T cell cytokine profile. Disease induction was achieved by active immunization with the peptide and adoptive transfer of peptide-activated T cells.

β-Tectorin 71-90 and Coch protein 131-150 induced a Th1-like effector immune responses in primed mice. Mice immunized with either β-tectorin 71-90 or Coch protein 131-150 showed increased hearing thresholds when compared to non-treated age- and sex- matched controls (p=0.010 and 0.024) and ovalbumin treated controls (p=0.012 and 0.017). Furthermore, increased hearing thresholds were observed in SWXJ mice after adoptive transfer of β-tectorin 71-90 or Coch protein 131-150 activated T cells (p=0.002 and 0.018).

β-Tectorin 71-90 and Coch protein 131-150 peptides induce Th1-like effector T cell immune responses in SWXJ mice. Active and passive immunization with these peptides induce hearing loss, which leads to the establishment of an inner ear-specific mouse model for ASNHL. These data show that Th1-like effector T cells may have a pivotal role in the etiopathogenesis of ASNHL.