Takeno M, Kariyone A, Yamashita N, Takiguchi M, Mizushima Y, Kaneoka H, Sakane T
St. Marianna University School of Medicine, Kawasaki, Japan.
Arthritis Rheum. 1995 Mar;38(3):426-33. doi: 10.1002/art.1780380321.
To elucidate the role played by HLA-B51 in the neutrophil hyperfunction of Behçet's disease, we determined the superoxide production by purified peripheral blood neutrophils from Behçet's disease patients, from HLA-B51 positive healthy individuals, and from HLA-B51 transgenic mice.
Neutrophil function was evaluated by flow cytometric analysis, detecting the conversion of 2',7'-dichlorofluorescin diacetate into dichloroflurescein, induced by superoxide in the neutrophils.
A significant correlation between the neutrophil hyperfunction and the possession of HLA-B51 phenotype, regardless of the presence of the disease, was observed in humans. FMLP-stimulated neutrophils (without in vitro priming) from HLA-B51 transgenic mice, but not those from HLA-B35 transgenic mice or from nontransgenic mice, produced substantial amounts of superoxide.
The HLA-B51 molecule itself may be responsible, at least in part, for neutrophil hyperfunction in Behçet's disease.
为阐明HLA - B51在白塞病中性粒细胞功能亢进中所起的作用，我们测定了白塞病患者、HLA - B51阳性健康个体以及HLA - B51转基因小鼠的纯化外周血中性粒细胞产生超氧化物的情况。
通过流式细胞术分析评估中性粒细胞功能，检测中性粒细胞中超氧化物诱导的二乙酸二氯荧光素向二氯荧光素的转化。
在人类中观察到，无论疾病是否存在，中性粒细胞功能亢进与HLA - B51表型的拥有之间存在显著相关性。来自HLA - B51转基因小鼠的FMLP刺激的中性粒细胞（无体外预刺激）产生大量超氧化物，而来自HLA - B35转基因小鼠或非转基因小鼠的中性粒细胞则不产生。
HLA - B51分子本身可能至少部分地导致了白塞病中性粒细胞功能亢进。
