ArticleInfection and immunity2002
Accumulation of human heat shock protein 60-reactive T cells in the gingival tissues of periodontitis patients.
Article in Infection and immunity, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 102 citations in OpenAlex.
- Is periodontitis triggering an inflammatory response in the liver, and does this reaction entail oxidative stress?Odontology · 2025Review
- Potential targets of phytochemical immunomodulatory therapy in periodontitis immunopathogenesis: A narrative review.The Saudi dental journal · 2023Review
- Comprehensive Pan-Cancer Analysis of Heat Shock Protein 110, 90, 70, and 60 Families.Frontiers in molecular biosciences · 2021Article
- Oral Dysbiosis and Autoimmunity: From Local Periodontal Responses to an Imbalanced Systemic Immunity. A Review.Frontiers in immunology · 2020Review
- Heat Shock Proteins in Cancer Immunotherapy.Journal of oncology · 2019Review
- Potential Impact of Oral Inflammations on Cardiac Functions and Atrial Fibrillation.Biomolecules · 2018Review
- Roles of Oral Infections in the Pathomechanism of Atherosclerosis.International journal of molecular sciences · 2018Review
- Interaction between periodontitis and liver diseases.Biomedical reports · 2016Article
- Periodontitis as a risk factor of atherosclerosis.Journal of immunology research · 2014Review
- Heat-shock protein 60 kDa and atherogenic dyslipidemia in patients with untreated mild periodontitis: a pilot study.Cell stress & chaperones · 2012Article
- Diabetes, periodontitis, and the subgingival microbiota.Journal of oral microbiology · 2010Article
- Cardiovascular disease and the role of oral bacteria.Journal of oral microbiology · 2010Article
- Relationship of periodontal infection to serum antibody levels to periodontopathic bacteria and inflammatory markers in periodontitis patients with coronary heart disease.Clinical and experimental immunology · 2007Article
- Balance of inflammatory response in stable gingivitis and progressive periodontitis lesions.Clinical and experimental immunology · 2006Article
- The immune responses to human and microbial heat shock proteins in periodontal disease with and without coronary heart disease.Clinical and experimental immunology · 2005Article
- A human oral keratinocyte cell line responds to human heat shock protein 60 through activation of ERK1/2 MAP kinases and up- regulation of IL-1beta.Clinical and experimental immunology · 2005Article
- Characterization of heat shock protein-specific T cells in atherosclerosis.Clinical and diagnostic laboratory immunology · 2005Article
- Heat shock protein and gliadin peptide promote development of peptidase antibodies in children with autism and patients with autoimmune disease.Clinical and diagnostic laboratory immunology · 2004Article
- Effect of periodontal treatment on the serum antibody levels to heat shock proteins.Clinical and experimental immunology · 2004Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
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.
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