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Role of Heat Shock Protein Derived from Streptococcus sanguinis in Behcet's Disease | OMICS International | Abstract
ISSN: 2161-0703

Journal of Medical Microbiology & Diagnosis
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Special Issue Article

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

Fumio Kaneko1*, Ari Togashi1, Erika Nomura1, Koichiro Nakamura2, Emiko Isogai3, Kenji Yokota4 and Keiji Oguma4

1Institute of Dermato-Immunology and Allergy, Southern Tohoku Research Institute for Neuroscience, Koriyama, Japan

2Department of Dermatology, Saitama Medical University, Saitama, Japan

3Laboratory Microbiology, Graduate School of Agricultural Science, Tohoku University, Sendai, Japan

4Department of Bacteriology, Okayama University Graduate School of Medicine and Dentistry, Medical School, Okayama, Japan

*Corresponding Author:
Fumio kaneko
Institute of Dermato-Immunology and Allergy
Southern Tohoku Research Institute for Neuroscience
Koriyama, Japan
E-mail: [email protected]

Received Date: November 09, 2011; Accepted Date: January 06, 2012; Published Date: January 11, 2012

Citation: Kaneko F, Togashi A, Nomura E, Nakamura K, Isogai E, et al. (2012) Role of Heat Shock Protein Derived from Streptococcus sanguinis in Behcet’s Disease. J Medical Microbiol Diagnosis S2:001. doi: 10.4172/2161-0703.S2-001

Copyright: © 2012 Kaneko F, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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.

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