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Infection and Immunity, May 2002, p. 2492-2501, Vol. 70, No. 5
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.5.2492-2501.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Accumulation of Human Heat Shock Protein 60-Reactive T Cells in the Gingival Tissues of Periodontitis Patients

Kazuhisa Yamazaki,1* Yutaka Ohsawa,1 Koichi Tabeta,1 Harue Ito,1 Kaoru Ueki,1 Taro Oda,1 Hiromasa Yoshie,1 and Gregory J. Seymour2

Division of Periodontology, Department of Oral Biological Science, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan,1 Oral Biology and Pathology, School of Dentistry, The University of Queensland, Brisbane, Australia2

Received 31 October 2001/ Returned for modification 2 January 2002/ Accepted 20 January 2002

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) ß-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.

* Corresponding author. Mailing address: Division of Periodontology, Department of Oral Biological Sciences, Niigata University Graduate School of Medical and Dental Sciences, 5274 Gakkocho 2-ban-cho, Niigata 951-8514, Japan. Phone: 81-25-227-2870. Fax: 81-25-227-0808. E-mail: kaz{at}dent.niigata-u.ac.jp.

Editor: W. A. Petri, Jr.

Infection and Immunity, May 2002, p. 2492-2501, Vol. 70, No. 5
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.5.2492-2501.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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