Previously we reported the capacity of the inner ear to respond immunologically by demonstrating a rise in perilymph antigen-specific antibody following inner ear sensitization. This rise in perilymph antibody was either the result of increased vascular permeability to serum immunoglobulins or the result of local antibody production. In order to determine if the inner ear was the source of antibody, a serum reference was established by systemically immunizing animals to bovine serum albumin (BSA). With anti-BSA as a serum marker during inner ear immunization with keyhole limpet hemocyanin (KLH), we were able to demonstrate an increase in anti-KLH perilymph antibody levels without a corresponding increase in anti-BSA levels. This suggested that increased vascular permeability was not responsible for the increased perilymph levels and that local production of antibody had occurred within the inner ear. The response was independent of the cerebrospinal fluid.