Behcet's Disease (Adamantiades-Behcet's Disease)

被引:44
|
作者
Kaneko, Fumio [1 ]
Togashi, Ari [1 ]
Saito, Sanae [1 ]
Sakuma, Hideo [2 ]
Oyama, Noritaka [3 ]
Nakamura, Koichiro [4 ]
Yokota, Kenji [5 ]
Oguma, Keiji [5 ]
机构
[1] So TOHOKU Res Inst Neurosci, Inst Dermatoimmunol & Allergy, Fukushima 9638563, Japan
[2] So TOHOKU Res Inst Neurosci, Div Pathol, Koriyama, Fukushima 9638563, Japan
[3] Fukushima Med Univ, Sch Med, Dept Dermatol, Fukushima 9601295, Japan
[4] Saitama Med Univ, Moroyama, Saitama 3500495, Japan
[5] Okayama Univ, Sch Med, Grad Sch Med & Dent, Dept Bacteriol, Okayama 7008558, Japan
关键词
HEAT-SHOCK-PROTEIN; TOXIN B-SUBUNIT; STREPTOCOCCUS-SANGUIS; T-CELLS; PEPTIDE; 336-351; TH1; CELLS; EXPRESSION; PATHOGENESIS; HYPERSENSITIVITY; ASSOCIATION;
D O I
10.1155/2011/681956
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Adamantiades-Behcet'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.
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页数:7
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