There is an increased rate of reported autoantibody production in patients with atopic and nonatopic asthma. The possibility of generating autoantibodies after the induction of immunotherapy can be explained by several mechanisms. One of these is immune deviation from TH2 to TH1 response by the effect of immunotherapy in favor of unregulated response to self-antigens. The other theory is a possible antigenic mimicry enabling autoantibody formation in these patients, Sixty-three atopic asthmatic children were included in the study. The patients were divided into three groups: Group 1: patients with atopic bronchial asthma without immunotherapy: Group 11: patients receiving immunotherapy for a maximum of 3 years; Group III: patients receiving immunotherapy for 4-5 years. The autoantibodies examined in the study population were antinuclear antibody, anti-double stranded DNA, rheumatoid factor, liver-kidney microsomal antibody, anti-mitochondrial antibody, anti-thyroglobulin and anti-microsomal antibody, anti-Smith antibody and lupus anticoagulant. An overall incidence of 17.5% autoantibody positivity was observed in patients, with no statistical significance between the treatment groups. IgG levels were significantly elevated in Group III when compared with Group 1. Based on these findings it is suggested, in accordance with other studies, that long-term immunotherapy in the pediatric age group does not cause a significant autoantibody formation other than the overall increased incidence that occurs in asthmatic patients.