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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
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.
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:
- 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.