title: Accumulation of human heat shock protein 60-reactive T cells in the gingival tissues of periodontitis patients.
abstract: Heat shock protein 60s (hsp60) are remarkably immunogenic, and both T-cell and antibody responses to hsp60 have been reported in various inflammatory conditions. To clarify the role of hsp60 in T-cell responses in periodontitis, we examined the proliferative response of peripheral blood mononuclear cells (PBMC), as well as the cytokine profile and T-cell clonality, for periodontitis patients and controls following stimulation with recombinant human hsp60 and Porphyromonas gingivalis GroEL. To confirm the infiltration of hsp60-reactive T-cell clones into periodontitis lesions, nucleotide sequences within complementarity-determining region 3 of the T-cell receptor (TCR) beta-chain were compared between hsp60-reactive peripheral blood T cells and periodontitis lesion-infiltrating T cells. Periodontitis patients demonstrated significantly higher proliferative responses of PBMC to human hsp60, but not to P. gingivalis GroEL, than control subjects. The response was inhibited by anti-major histocompatibility complex class II antibodies. Analysis of the nucleotide sequences of the TCR demonstrated that human hsp60-reactive T-cell clones and periodontitis lesion-infiltrating T cells have the same receptors, suggesting that hsp60-reactive T cells accumulate in periodontitis lesions. Analysis of the cytokine profile demonstrated that hsp60-reactive PBMC produced significant levels of gamma interferon (IFN-gamma) in periodontitis patients, whereas P. gingivalis GroEL did not induce any skewing toward a type1 or type2 cytokine profile. In control subjects no significant expression of IFN-gamma or interleukin 4 was induced. These results suggest that periodontitis patients have human hsp60-reactive T cells with a type 1 cytokine profile in their peripheral blood T-cell pools.
authors.affiliation: Division of Periodontology, Department of Oral Biological Science, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan. kaz@dent.niigata-u.ac.jp
authors.forename: Kazuhisa
authors.initials: K
authors.lastname: Yamazaki
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Ohsawa
authors.forename: Koichi
authors.initials: K
authors.lastname: Tabeta
authors.forename: Harue
authors.initials: H
authors.lastname: Ito
authors.forename: Kaoru
authors.initials: K
authors.lastname: Ueki
authors.forename: Taro
authors.initials: T
authors.lastname: Oda
authors.forename: Hiromasa
authors.initials: H
authors.lastname: Yoshie
authors.forename: Gregory J
authors.initials: GJ
authors.lastname: Seymour
mesh_terms: D000328:Adult; D001483:Base Sequence; D018834:Chaperonin 60 / Q000276:immunology*; D005881:Gingiva / Q000276:immunology*; D006684:HLA-DR Antigens / Q000502:physiology; D006801:Humans; D007371:Interferon-gamma / Q000096:biosynthesis; D018664:Interleukin-12 / Q000096:biosynthesis; D008213:Lymphocyte Activation; D008875:Middle Aged; D010518:Periodontitis / Q000276:immunology*; D018807:Polymorphism, Single-Stranded Conformational; D016966:Porphyromonas gingivalis / Q000276:immunology*; D016693:Receptors, Antigen, T-Cell, alpha-beta / Q000235:genetics; D013601:T-Lymphocytes / Q000276:immunology*
chemical_list: D018834:Chaperonin 60; D006684:HLA-DR Antigens; D016693:Receptors, Antigen, T-Cell, alpha-beta; D018664:Interleukin-12; D007371:Interferon-gamma