title: IgG reactive to CTL-directed epitopes of self-antigens is either lacking or unbalanced in atopic dermatitis patients.
abstract: We previously demonstrated that CTL-directed epitopes derived from non-mutated self-antigens elicit a type-I allergy in the majority of healthy donors (HD) as did the presence of IgE and IgG reactive to these peptides in the sera of the donors. We investigated in this study whether Igs reactive to eight types of CTL-directed peptides were elevated in the sera of 40 patients with atopic dermatitis (AD). Total IgE levels in the sera of AD patients were significantly higher than those of HD, however, no significant differences between the AD patients and the HD were observed in either the serum levels or the positive rates of IgE reactive to seven of the eight peptides. Total IgG levels were not different from each other, however, IgG reactive to the two peptides with no sequence similarity to other species and one peptide that had similarity to DNA helicase II of enterobacteria were not detectable in the sera of the AD patients. Although IgG reactive to the remaining five peptides, which had sequence similarity to other species, were detectable in both the AD patients and the HD, ratios of peptide-specific IgG1/IgG2 were mostly lower in the AD patients than in the HD. These results indicate that IgG reactive to CTL-directed epitopes of self-antigens is either lacking or unbalanced in AD patients. This information may provide new insight into the immune-mechanisms of elevated auto-reactivity of AD patients.
authors.affiliation: Cancer Vaccine Development Division, Kurume University Research Center for Innovative Cancer Therapy, Kurume, Japan.
authors.forename: N
authors.initials: N
authors.lastname: Kawamoto
authors.forename: A
authors.initials: A
authors.lastname: Yamada
authors.forename: S
authors.initials: S
authors.lastname: Ohkouchi
authors.forename: T
authors.initials: T
authors.lastname: Maeda
authors.forename: S
authors.initials: S
authors.lastname: Tanaka
authors.forename: T
authors.initials: T
authors.lastname: Hashimoto
authors.forename: Y
authors.initials: Y
authors.lastname: Saijo
authors.forename: S
authors.initials: S
authors.lastname: Saijo
authors.forename: T
authors.initials: T
authors.lastname: Nukiwa
authors.forename: S
authors.initials: S
authors.lastname: Shichijo
authors.forename: H
authors.initials: H
authors.lastname: Aizawa
authors.forename: K
authors.initials: K
authors.lastname: Itoh
mesh_terms: D036002:ADP Ribose Transferases / Q000276:immunology; D000293:Adolescent; D000328:Adult; D000951:Antigens, Neoplasm / Q000276:immunology; D001324:Autoantigens / Q000097:blood / Q000276:immunology*; D016022:Case-Control Studies; D002648:Child; D021983:Cyclophilins / Q000276:immunology; D004268:DNA-Binding Proteins / Q000276:immunology; D003876:Dermatitis, Atopic / Q000097:blood / Q000276:immunology*; D000939:Epitopes; D005260:Female; D006801:Humans; D007073:Immunoglobulin E / Q000145:classification / Q000276:immunology; D007074:Immunoglobulin G / Q000145:classification / Q000276:immunology*; D008297:Male; D008565:Membrane Proteins / Q000276:immunology; D009363:Neoplasm Proteins / Q000276:immunology; D010446:Peptide Fragments / Q000276:immunology*; D019696:Peptidylprolyl Isomerase; D016601:RNA-Binding Proteins / Q000276:immunology; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology*
chemical_list: D000951:Antigens, Neoplasm; D001324:Autoantigens; D004268:DNA-Binding Proteins; D000939:Epitopes; D007074:Immunoglobulin G; D008565:Membrane Proteins; D009363:Neoplasm Proteins; D010446:Peptide Fragments; D016601:RNA-Binding Proteins; C416530:SART3 protein, human; C081786:cyclophilin B; D007073:Immunoglobulin E; D036002:ADP Ribose Transferases; C105234:ART4 protein, human; C405383:DSE protein, human; D021983:Cyclophilins; D019696:Peptidylprolyl Isomerase