ArticleImmunology2000
Relationship between disease severity and responses by blood mononuclear cells from patients with rheumatoid arthritis to human heat-shock protein 60.
Article in Immunology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 53 citations in OpenAlex.
- The danger from within: alarmins in arthritis.Nature reviews. Rheumatology · 2016Review
- Opposing roles for heat and heat shock proteins in macrophage functions during inflammation: a function of cell activation state?Frontiers in immunology · 2012Article
- A signature of aberrant immune responsiveness identifies myocardial dysfunction in rheumatoid arthritis.Arthritis and rheumatism · 2011Article
- The involvement of heat-shock proteins in the pathogenesis of autoimmune arthritis: a critical appraisal.Seminars in arthritis and rheumatism · 2010Review
- Analysis of complex biomarkers for human immune-mediated disorders based on cytokine responsiveness of peripheral blood cells.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
- Short-term hyperthermia prevents activation of proinflammatory genes in fibroblast-like synoviocytes by blocking the activation of the transcription factor NF-kappaB.Journal of molecular medicine (Berlin, Germany) · 2006Article
- Heat-shock proteins induce T-cell regulation of chronic inflammation.Nature reviews. Immunology · 2005Review
- Facets of heat shock protein 70 show immunotherapeutic potential.Immunology · 2003Review
- Accumulation of human heat shock protein 60-reactive T cells in the gingival tissues of periodontitis patients.Infection and immunity · 2002Article
- Self heat-shock protein 65-mediated regulation of autoimmune arthritis.Journal of autoimmunityArticle
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The hypothesis that T-cell responses to the 60 000 MW family of heat-shock proteins (hsp) may be related to the severity of rheumatoid arthritis (RA) was examined. Peripheral blood mononuclear cells (PBMC) from most normal individuals and both early and established RA patients proliferated in vitro in response to human hsp 60 and mycobacterial hsp 65 as well as tetanus toxoid (TT) and mycobacterial purified protein derivative (PPD). PBMC from some patients with established RA gave responses to hsp 60 that were above the normal range and/or peaked earlier than PBMC from normal individuals. The responses of PBMC from established RA to hsp 65, but not PPD or TT, were also higher than those from normal individuals, but the peak responses to all three antigens appeared delayed. Thus a selective increase in responsiveness to hsp 60 develops with disease duration in many RA patients. Six assessments of disease activity and severity were made but apart from rheumatoid factor titre, they were unrelated to the proliferative response. Similarly, disease activity and severity did not differ between those RA patients whose hsp 60 stimulated cells produced interferon-gamma and those who did not, although patients whose hsp 60-stimulated T cells produced interleukin-4 (IL-4) and/or IL-10, appeared to have less disease activity and severity than those who did not. Significant negative correlations were found between IL-10 production by hsp 60-stimulated cells and disease assessments. It is considered that RA is less severe in those patients whose hsp 60-stimulated cells produce T-helper 2 type cytokines.
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Registered trials
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