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Clinical and Developmental Immunology
Volume 2011, Article ID 681956, 7 pages
http://dx.doi.org/10.1155/2011/681956
Review Article

Behçet's Disease (Adamantiades-Behçet's Disease)

1Institute of Dermato-Immunology and Allergy, Southern TOHOKU Research Institute for Neuroscience, 7-115 Yatsuyamada, Koriyama, Fukushima 963-8563, Japan
2Pathology Division, Southern TOHOKU Research Institute for Neuroscience, 7-115 Yatsuyamada, Koriyama 963-8563, Japan
3Departments of Dermatology, School of Medicine, Fukushima Medical University, Hikarigaoka-1, Fukushima 960-1295, Japan
4Saitama Medical University, 38 Hongo, Moroyama, Iruma-gun, Saitama 350-0495, Japan
5Department of Bacteriology, Graduate School of Medicine and Dentistry, Medical School, Okayama University, 5-1, Shikata-cho-2, Okayama 700-8558, Japan

Received 13 May 2010; Accepted 7 September 2010

Academic Editor: Fang-Ping Huang

Copyright © 2011 Fumio Kaneko et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Adamantiades-Behçet's disease (ABD) is characterized by starting with oral aphthous ulceration and developing of the systemic involvements. The pathogenesis of ABD is closely correlated with the genetic factors and the triggering factors which acquire delayed-type hypersensitivity reaction against oral streptococci mediated by IL-12 cytokine family. HLA-B51 is associated in more than 60% of the patients and its restricted CD8+ T cell response is clearly correlated with the target tissues. Bes-1 gene encoded partial S. sanguinis genome which is highly homologous with retinal protein, and 65 kD heat shock protein (Hsp-65) released from streptococci is playing an important role with human Hsp-60 in the pathogenesis of ABD. Although Hsp-65/60 has homologies with the respective T cell epitope, it stimulates peripheral blood mononuclear cells (PBMCs) from ABD patients. On the other hand, some peptides of Hsp-65 were found to reduce IL-8 and IL-12 production from PBMCs of ABD patients in active stage.