title: Selective expansion of T cells in gingival lesions of patients with chronic inflammatory periodontal disease.
abstract: Chronic inflammatory periodontal diseases are characterized by a cellular infiltrate and are similar in many respects to other chronic inflammatory diseases. While periodontopathic bacteria have been recognized as the principal causative agent and the immune response to these bacteria is thought to be responsible for the tissue destruction, the full aetiological spectrum is still incompletely understood. In addition to many cell types such as polymorphonuclear leucocytes and macrophages, T cells have been implicated in pathogenesis and are considered to have regulatory roles in progression of the disease. Based on our recent studies demonstrating biased expression of several Vbeta families in periodontitis tissues, the aim of this study was to characterize further the T cells relevant to the disease process by reverse transcription-polymerase chain reaction-single-strand conformation polymorphism (RT-PCR-SSCP) and subsequent nucleotide sequence analysis of complementarity-determining region 3 (CDR3) of the TCR beta-chain. In spite of the likely involvement of numerous bacteria, the present study has clearly shown the oligoclonality of infiltrating T cells in periodontitis lesions in contrast to low clonality of peripheral blood T cells as evidenced by the appearance of distinct bands in gingival tissue samples and smear pattern of peripheral blood on SSCP gels. These were confirmed by the DNA sequencing of the CDR3 of Vbeta16 of selected samples. The analysis of deduced amino acid sequences demonstrated amino acid motifs in the CDR3 region of the periodontitis lesion-derived sequences from each patient. The results indicate that gingival tissue-infiltrating T cells recognizing a limited number of antigens or epitopes are involved in the disease process.
authors.affiliation: Department of Periodontology, Faculty of Dentistry, Niigata University, Niigata, Japan. kaz@dent.niigata-u.ac.jp
authors.forename: K
authors.initials: K
authors.lastname: Yamazaki
authors.forename: T
authors.initials: T
authors.lastname: Nakajima
authors.forename: Y
authors.initials: Y
authors.lastname: Ohsawa
authors.forename: K
authors.initials: K
authors.lastname: Tabeta
authors.forename: H
authors.initials: H
authors.lastname: Yoshie
authors.forename: K
authors.initials: K
authors.lastname: Sakurai
authors.forename: G J
authors.initials: GJ
authors.lastname: Seymour
mesh_terms: D000328:Adult; D000368:Aged; D000595:Amino Acid Sequence; D002455:Cell Division / Q000235:genetics / Q000276:immunology; D002465:Cell Movement / Q000235:genetics / Q000276:immunology; D002908:Chronic Disease; D002999:Clone Cells; D015333:Gene Rearrangement, beta-Chain T-Cell Antigen Receptor / Q000276:immunology; D019674:Genes, T-Cell Receptor beta; D005881:Gingiva / Q000166:cytology / Q000276:immunology / Q000473:pathology*; D005891:Gingivitis / Q000276:immunology* / Q000473:pathology*; D006801:Humans; D008213:Lymphocyte Activation / Q000235:genetics / Q000276:immunology*; D008875:Middle Aged; D008969:Molecular Sequence Data; D010518:Periodontitis / Q000276:immunology* / Q000473:pathology*; D016693:Receptors, Antigen, T-Cell, alpha-beta / Q000235:genetics; D013601:T-Lymphocytes / Q000276:immunology* / Q000378:metabolism
chemical_list: D016693:Receptors, Antigen, T-Cell, alpha-beta