Ann Rheum Dis 2001;60:996-1002 ( November )

R eview

Behçet's disease: infectious aetiology, new autoantigens, and HLA-B51

H Direskeneli

Division of Rheumatology, Faculty of Medicine, Marmara University, Istanbul, Turkey

Correspondence to: Dr H Direskeneli, Resit Pasa Sok. 36/5, Kiziltoprak, Kadiköy Istanbul, Turkey haner@marun.edu.tr

Accepted for publication 25 April 2001

The first 150 words of the full text of this article appear below.

	Introduction

Behçet's disease (BD) is a multisystemic disorder with mucocutaneous, ocular, arthritic, vascular, and central nervous system involvements.¹ Recent developments in the immunopathogenesis of BD are discussed in this review. Box 1 summarises the major aspects covered.

Figure Removed (Available Only in the Full Text)

	Neutrophil activation

Neutrophils are mature immune cells with a very short life in vitro and have a pivotal role in innate immune responses. As typical BD lesions such as pustular folliculitis, pathergy reactions, and hypopyon have significant neutrophil infiltrations, neutrophil functions and activation status have been extensively investigated.^1 2 Conflicting reports of increased, normal, or decreased basal and fMLP stimulated superoxide productions, phagocytosis, chemotaxis, and neutrophil-endothelial adhesion in BD may reflect the status of clinical activity, in vivo neutrophil activation, drug effects, or just methodological problems of investigating neutrophils.^3-9 In a recent study, which showed decreased fMLP stimulated superoxide production in BD and patients with sepsis, consecutive restimulations of prestimulated BD neutrophils produced a smaller increase in . . . [Full text of this article]

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

• Atzeni, F., Boiardi, L., Casali, B., Farnetti, E., Sarzi-Puttini, P., Pipitone, N., Olivieri, I., Cantini, F., Salvi, F., La Corte, R., Triolo, G., Filippini, D., Paolazzi, G., Salvarani, C. (2007). Lack of association of the 463 G/A myeloperoxidase promoter polymorphism with Behcet's disease in Italian patients. Rheumatology (Oxford) 46: 1547-1550 [Abstract] [Full Text]  
• Suzuki, N., Nara, K., Suzuki, T. (2006). Skewed Th1 Responses Caused by Excessive Expression of Txk, a Member of the Tec Family of Tyrosine Kinases, in Patients with Behcet's Disease.. Clin Med Res 4: 147-151 [Abstract] [Full Text]  
• Ahn, J. K., Chung, H., Lee, D.-s., Yu, Y. S., Yu, H. G. (2005). CD8brightCD56+ T Cells Are Cytotoxic Effectors in Patients with Active Behcet's Uveitis. J. Immunol. 175: 6133-6142 [Abstract] [Full Text]  
• Ahn, J. K., Seo, J.-M., Yu, J., Oh, F. S., Chung, H., Yu, H. G. (2005). Down-Regulation of IFN-{gamma}-Producing CD56+ T Cells after Combined Low-Dose Cyclosporine/Prednisone Treatment in Patients with Behcet's Uveitis. IOVS 46: 2458-2464 [Abstract] [Full Text]  
• Schaerli, P., Britschgi, M., Keller, M., Steiner, U. C., Steinmann, L. S., Moser, B., Pichler, W. J. (2004). Characterization of Human T Cells That Regulate Neutrophilic Skin Inflammation. J. Immunol. 173: 2151-2158 [Abstract] [Full Text]  
• Mumcu, G., Ergun, T., Inanc, N., Fresko, I., Atalay, T., Hayran, O., Direskeneli, H. (2004). Oral health is impaired in Behcet's disease and is associated with disease severity. Rheumatology (Oxford) 43: 1028-1033 [Abstract] [Full Text]  
• Saruhan-Direskeneli, G., Uyar, F. A., Cefle, A., Onder, S. C., Eksioglu-Demiralp, E., Kamali, S., Inanc, M., Ocal, L., Gul, A. (2004). Expression of KIR and C-type lectin receptors in Behcet's disease. Rheumatology (Oxford) 43: 423-427 [Abstract] [Full Text]  
• Schmid, S., Kuechler, P. C., Britschgi, M., Steiner, U. C., Yawalkar, N., Limat, A., Baltensperger, K., Braathen, L., Pichler, W. J. (2002). Acute Generalized Exanthematous Pustulosis: Role of Cytotoxic T Cells in Pustule Formation. Am. J. Pathol. 161: 2079-2086 [Abstract] [Full Text]