Excessive function of peripheral blood neutrophils from patients with behcet's disease and from hla-b51 transgenic mice
Version of Record online: 9 DEC 2005
Copyright © 1995 American College of Rheumatology
Arthritis & Rheumatism
Volume 38, Issue 3, pages 426–433, March 1995
How to Cite
Takeno, M., Kariyone, A., Yamashita, N., Takiguchi, M., Mizushima, Y., Kaneoka, H. and Sakane, T. (1995), Excessive function of peripheral blood neutrophils from patients with behcet's disease and from hla-b51 transgenic mice. Arthritis & Rheumatism, 38: 426–433. doi: 10.1002/art.1780380321
- Issue online: 9 DEC 2005
- Version of Record online: 9 DEC 2005
- Manuscript Revised: 5 OCT 1994
- Manuscript Accepted: 5 OCT 1994
- Manuscript Received: 13 APR 1994
- Behcet's Disease Research Committee
- Ministry of Health and Welfare of
- Uehara Memorial Foundation
- Kanagawa Nanbyo Foundation
- Japan Intractable Diseases Research Foundation
Objective. To elucidate the role played by HLA-B51 in the neutrophil hyperfunction of Behcet's disease, we determined the superoxide production by purified peripheral blood neutrophils from Behcet's disease patients, from HLA-B51 positive healthy individuals, and from HLA-B51 transgenic mice.
Methods. Neutrophil function was evaluated by flow cytometric analysis, detecting the conversion of 2′,7′-dichlorofluorescin diacetate into dichlorofluorescein, induced by superoxide in the neutrophils.
Results. 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.
Conclusion. The HLA-B51 molecule itself may be responsible, at least in part, for neutrophil hyper-function in Behcst's disease.