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Related Experiment Videos

Defining a T-cell epitope within HSP 65 in recurrent aphthous stomatitis.

A Hasan1, T Shinnick, Y Mizushima

  • 1Department of Periodontology and Preventive Dentistry, GKT Dental Institute, London, UK. adam.hasan@kcl.ac.uk

Clinical and Experimental Immunology
|May 3, 2002
PubMed
Summary

Mycobacterial heat shock protein (HSP) 65-derived peptide 95-105 specifically stimulates T cells in recurrent aphthous stomatitis (RAS) patients. This immune response may trigger the condition by cross-reacting with human HSP 60.

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Area of Science:

  • Immunology
  • Molecular Biology
  • Dermatology

Background:

  • Recurrent aphthous stomatitis (RAS) is linked to 65 kD heat shock protein (HSP).
  • Previous studies showed mycobacterial HSP 65 peptide 91-105 stimulates RAS patient lymphocytes.

Purpose of the Study:

  • Investigate T cell responses to mycobacterial and human HSP peptides in RAS.
  • Identify specific peptide regions and T cell subsets involved in RAS pathogenesis.

Main Methods:

  • Lymphocyte stimulation assays using mycobacterial and human HSP peptides.
  • T cell subset analysis (CD4+, CD8+) and MHC restriction studies (class I, class II).
  • Peptide truncation and substitution to identify critical residues.

Main Results:

Related Experiment Videos

  • Mycobacterial peptide 91-105 stimulated both CD4+ and CD8+ T cells.
  • Human homologous peptide 116-130 stimulated only CD4+ T cells.
  • Peptide residues 95-105, particularly Arg104, are critical for T cell stimulation.

Conclusions:

  • Peptide 95-105 from microbial HSP 65 may act as a T-cell epitope in RAS.
  • A cross-reactive immune response to human HSP 60, initiated by microbial HSP, is postulated to cause RAS.