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

A Hasan, T Shinnick, Y Mizushima, R Van der Zee, T Lehner

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40 Citations (Scopus)


The 65 kD heat shock protein (HSP) has been implicated in the aetiology of recurrent aphthous stomatitis (RAS). We have previously demonstrated that peptide 91-105 derived from the sequence of mycobacterial 65 kD HSP stimulates specifically lymphocytes from patients with RAS. In this investigation, we show that both CD4(+) and CD8(+) T cells were significantly stimulated with mycobacterial peptide 91-105. In contrast, the human homologous peptide 116-130 stimulated only CD4(+) T cells. Inhibition studies showed that CD4(+) T cells were class II restricted, whereas CD8(+) T cells were class I restricted. We then used truncated or substituted peptides, and demonstrated that residues 95-105 appear to be important, and residue 104(Arg) critical, in stimulating the T cells. Thus, peptide 95105 may constitute a T-cell proliferative epitope in RAS. We postulate that the high load of microorganisms that colonize the oral mucosa may initiate an immune response by the microbial HSP 65-derived peptide 95-105, stimulating the numerous Langerhans cells in the oral mucosa to activate a cross-reacting immune response to the homologous peptide 116-130 within the epithelial HSP 60 initiating the immunopathological changes that lead to RAS.
Original languageEnglish
Pages (from-to)318 - 325
Number of pages8
JournalClinical and Experimental Immunology
Issue number2
Publication statusPublished - 2002


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