Type I allergic rhinitis, an inflammatory condition of upper airways, often impairs quality of life of sufferers, even though it is not a life-threatening disease (25). For example, the disease results in decreased productivity and potential absenteeism from work or schooling (2). Prevalence of allergic rhinitis appears to be increasing. Possible factors for this would be increases in airborne pollution, increases in dust mite populations, changes in living and dietary conditions, control of infectious diseases and vaccinations (4,15,22,23).On pathogenesis of allergic rhinitis, major interest has been centered on immunological disorders of massive production of allergen-specific IgE antibodies and proallergic mediators including histamine (9, 15). However, the role of autoimmunity has been also implicated recently (16,21,24,26,27). Specifically, autoantibodies to IgE and β2-adrenergic receptors were reported in patients with allergic rhinitis (24, 27). Possible pathological roles of these autoantibodies have not been confirmed yet; rather, it remains even to be resolved whether autoimmunity in allergic rhinitis is directed selectively to IgE and/or β2-adrenergic receptors or directed to a wide range of self proteins. To address this question here we surveyed autoantibodies/autoantigens in allergic rhinitis using a proteomic approach. Specifically, proteins extracted from human peripheral blood mononuclear cells (PBMC) were separated by two-dimensional electrophoresis (2DE), and then were subjected to western blotting (WB) with serum samples from patients with allergic rhinitis. Then detected autoantigens were identified by mass fingerprinting. One of the identified proteins was found to be β-tubulin isoform V (β-tubV), which was found to be recognized as an autoantigen in 52% of the tested patients with allergic rhinitis by WB using recombinant β-tubV. Abstract: Autoantibodies to IgE and 2-adrenergic receptor have been reported in patients with allergic rhinitis. To investigate whether autoimmunity in allergic rhinitis is directed to such limited molecules or directed to a wide range of self proteins, we here attempted to survey autoantigens/autoantibodies comprehensively, using proteomics. Specifically, we separated proteins extracted from peripheral blood mononuclear cells by 2-dimensional electrophoresis and then detected autoantigens by subsequent western blotting with sera from patients with allergic rhinitis. As a result, we detected multiple autoantigens, some of which were further identified by mass fingerprinting. Next, we confirmed antigenicity of one of the identified autoantigens, -tubulin isoform V (-tubV), using a recombinant protein and then measured prevalence of the anti--tubV autoantibodies. As a result, 52% of the tested patients with allergic rhinitis were found to possess anti--tubV autoantibodies. Our study indicates that autoimmunity is a common phenomena and -tubV is one of the major autoantigens in allergic rhinitis.
Identification of -Tubulin