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Neutrophil CD64 Expression in Behçet's Disease

KEMAL ÜRETEN, IHSAN ERTENLI, M. AKIF ÖZTÜRK, SEDAT KIRAZ, A. MESUT ONAT, MURAT TUNCER, HAMZA OKUR, ALI AKDOGAN, SULE APRAS, and MERAL ÇALGÜNERI

ABSTRACT.

Objective.
Hyperfunction of neutrophils is a characteristic finding in Behçet's disease (BD). Microbial agents have been proposed as causative agents in the disease flares. Fc gamma receptor 1 (CD64) is not normally expressed by neutrophils of healthy individuals, but is upregulated by these cells in response to microbial wall components and proinflammatory cytokines. The degree of polymorphonuclear leukocyte (PMN) CD64 expression is different in autoimmune diseases and systemic infectious diseases. We investigated PMN CD64 expression in patients with BD.

Methods. Thirty-seven patients with active BD (M/F: 18/19, mean age: 34.4 ± 9.7 yrs), 35 patients with inactive BD (M/F: 11/24, mean age: 35.9 ± 11.6 yrs), 27 patients with culture proven infections (M/F: 19/8, mean age: 54.4 ± 15.2 yrs), 31 healthy controls (M/F: 14/17, mean age: 37.7 ± 8.7 yrs), and 42 patients with active inflammatory disease (M/F: 13/29, mean age: 39.3 ± 14.9 yrs) were enrolled in this study. Flow cytometry was used to assess the prevalence of CD64-bearing PMN in whole blood samples.

Results. The prevalence of CD64-bearing PMN was significantly higher in patients with infectious disease (77.1 ± 18.4), inflammatory disease (37.1 ± 27.5), and active BD (48.9 ± 22.5) than in healthy controls (9.5 ± 7.8) or patients with inactive BD (12.9 ± 9.5). CD64 expression was similar in controls and patients with inactive BD. In the infectious disease group, expression of CD64 was significantly higher than in the active BD and active inflammatory disease groups, while there was no significant difference between the groups of patients with active BD and inflammatory disorders.

Conclusion. Neutrophil CD64 expression increases during exacerbation of BD. This increase appears to be a non-specific inflammatory response and does not reflect PMN activation triggered by a living microorganism. (J Rheumatol 2005;32:849-52)

Key Indexing Terms:

BEHÇET'S DISEASE
DISEASE ACTIVATION
CD64
NEUTROPHIL


From the Departments of Rheumatology and Pediatric Hematology, Hacettepe University School of Medicine; and the Department of Rheumatology, Gazi University School of Medicine, Ankara, Turkey.

K. Üreten, MD; I. Ertenli, MD, Department of Rheumatology, Hacettepe University; M.A. Öztürk, MD, Department of Rheumatology, Gazi University School of Medicine; S. Kiraz, MD; A.M. Onat, MD, Department of Rheumatology; M. Tuncer, MD; H. Okur, PhD, Department of Pediatric Hematology; A. Akdogan, MD; S. Apras, MD; M. Çalgüneri, MD, Department of Rheumatology, Hacettepe University.

Address reprint requests to Dr. M.A. Öztürk, Ostim mahallesi, 89. sokak, AK-84 sitesi, A-2 blok, no: 8, Yenimahalle, Ankara, 06170 Turkey. E-mail:makifozturk@yahoo.com

Accepted for publication December 20, 2004.




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