Accumulation of human heat shock protein 60-reactive T cells in the gingival tissues of periodontitis patients

Yamazaki, K., Ohsawa, Y., Tabeta, K., Ito, H., Ueki, K., Oda, T., Yoshie, H. and Seymour, G. J. (2002) Accumulation of human heat shock protein 60-reactive T cells in the gingival tissues of periodontitis patients. Infection And Immunity, 70 5: 2492-2501.


Author Yamazaki, K.
Ohsawa, Y.
Tabeta, K.
Ito, H.
Ueki, K.
Oda, T.
Yoshie, H.
Seymour, G. J.
Title Accumulation of human heat shock protein 60-reactive T cells in the gingival tissues of periodontitis patients
Journal name Infection And Immunity   Check publisher's open access policy
ISSN 0019-9567
Publication date 2002
Sub-type Article (original research)
DOI 10.1128/IAI.70.5.2492-2501.2002
Volume 70
Issue 5
Start page 2492
End page 2501
Total pages 10
Editor Fischetti, V. A.
O'Brien, A. D.
Place of publication USA
Publisher American Society for Microbiology
Collection year 2002
Language eng
Subject C1
320899 Dentistry not elsewhere classified
730112 Oro-dental and disorders
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 11 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 I cytokine profile in their peripheral blood T-cell pools.
Keyword Immunology
Infectious Diseases
Lymphocyte-associated Antigen-4
Blood Mononuclear-cells
Porphyromonas-gingivalis
Rheumatoid-arthritis
Immunological Characterization
Mycobacterium-tuberculosis
Autoimmune-disease
64-kda Protein
Synovial-fluid
Tolerance
Q-Index Code C1

Document type: Journal Article
Sub-type: Article (original research)
Collections: Excellence in Research Australia (ERA) - Collection
School of Dentistry Publications
 
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