The enhanced immune reaction associated with IGHG1 could be explained in several ways. First, an immune complex autoimmune disorder could explain this occurrence. Circulating Remdesivir autoantibodies to immunoglobulins could form immune complexes that may cause inner ear damage via a type III hypersensitivity reaction. Indeed, several studies have reported elevated circulating immune complexes in 54–94% of patients with Meniere’s disease. However, other studies have shown evidence of circulating immune complexes in only 4–7.4% of patients. Several methods can be used to detect circulating immune complexes; however, none of these methods can detect all types of circulating immune complexes. Therefore, the prevalence of patients with circulating immune complexes may vary from study to study. Differences in the race and number of patients enrolled in a study can also influence the prevalence of circulating immune complexes. Evidence of damage to the inner ear associated with circulating immune complexes is important in the pathogenesis of Meniere’s disease. However, evidence for inner ear pathology is insufficient, even though histopathological studies of the human temporal bone have demonstrated that patients with Meniere’s disease have C3 and C1q deposits in their inner ear. Second, increased amounts of anti-IGHG1 antibodies in patients with Meniere’s disease may be a result of an excessive autoimmune or inflammatory reaction in the inner ear. It is also possible that increased concentrations of anti-IGHG1 antibody are involved in regulating the immune system and suppressing excessive immune reactions by reducing B cell activity. Other antibodies may cause autoimmune reactions at a cellular level and affect the function of the epithelial cells of the inner ear that regulate inner ear homeostasis via the disruption of cell signaling or cellular structures. Such autoimmune reactions could result in secondary increases in the concentrations of anti-immunoglobulin antibodies. Demonstrating the presence of immune reaction between circulating autoantibodies in the serum and the inner ear tissue is important. We used western blots with proteins from mouse inner ear tissue and patient serum to demonstrate the existence of this type of immune reaction. The western blots showed that more antigen-antibody reactions occurred in the patients with Meniere’s disease than in the controls. Animal inner ear antigens that have been reported to react with sera from patients with Meniere’s disease have molecular weights in the 32–35 kDa, 42–46 kDa, 52– 59 kDa, and 79–80 kDa ranges. Microsequencing showed that the 28 KDa and 42 KDa antigens corresponded to Raf-1 and beta actin, respectively.