Authors: Salih Pay İsmail Şimşek Hakan Erdem Ayhan Dinç
Publish Date: 2006/12/14
Volume: 27, Issue: 5, Pages: 417-424
Abstract
Behçet’s disease BD is a systemic vasculitis with unclear etiology and pathogenesis Although several viral and bacterial causes have been investigated in detail for several years of late it is widely accepted that microorganisms may play a role as a trigger or as a crossreactive antigens that interfere with selfantigens such as heatshock proteins Genes such as HLAB51 MICA and TNF considered to play a crucial role in the pathogenesis of BD are located in the major histocompatibility complex MHC However it has been accepted that only HLAB51 is directly related with pathogenesis of the disease and others have strong linkage disequilibrium with HLAB51 Some other genes such as IL1 Factor V and ICAM1 KIR and eNOS assumed to take a part in the pathogenesis are settled out of the MHC region In patients with BD several abnormalities in innate and acquired immunity were detected Mainly the hypersensitivity of T lymphocytes to different types of antigens plays a critical role in the pathogenesis However it is not clear that whether defective signal transduction or antigen presenting cell APC dysfunction is responsible for T cell hypersensitivity Cytokines and chemokines secreted from APCs and T cells are suggested to cause the neutrophil hyperactivation Activated neutrophils secrete some cytokines which prime themselves and also stimulate Th1 cells These relationships among APCs Th1 lymphocytes and neutrophils constitute the basis of immune responses in BD In this review we focus on the possible role of APC in the pathogenesis of BD with an attempt to take attention of researchers in this field to these cells at the crossroads of innate and adaptive immunity and discuss other potential contributors including cells of the immune system and mediators
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