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Defining a T‐cell epitope within HSP 65 in recurrent aphthous stomatitis
SUMMARY 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 investi...
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Published in: | Clinical and experimental immunology 2002-05, Vol.128 (2), p.318-325 |
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Main Authors: | , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | SUMMARY
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 95– 105 may constitute a T‐cell proliferative epitope in RAS. We postulate that the high load of micro‐organisms 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. |
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ISSN: | 0009-9104 1365-2249 |
DOI: | 10.1046/j.1365-2249.2002.01757.x |