Role of Heat Shock Protein Derived from Streptococcus sanguinis in Behcet?s Disease

Abstract

Patients with Behcet’s disease (BD) have hypersensitivity against oral streptococci increased in their oral cavity. Heat shock protein-65/60 (Hsp-65/60) derived from S. sanguinis and the damaged mammalian tissues, respectively, are supposed to play an important role in BD pathogenesis. The antigen presenting cells taken Hsp-65 via Toll-like receptors in the oral lesion are carried to the local lesions by blood flow and they are known to lead T cells undergo apoptosis in the regional delayed type hypersensitive reaction. The human Hsp-60 peptide (336-351 aa) combined with recombinant cholera toxin B subunit was reported to be a therapeutic agent for BD patients with advanced uveitis. Here, we recognized that the peptide (249-264 aa; designated LO1 and 311-326aa: UK) of Hsp-65/60 exhibiting highly homologous to the T cell-epitope lead CD4+ and CD8+ T cell apoptosis in peripheral blood mononuclear cells from BD patients. In BD patients IL-8 and IL-12 production from activated T cells was significantly inhibited by LO1 and UK peptides. The results suggest that the peptides of Hsp-65/60 are able to be therapeutic agents for active BD patients.