Pathogenesis of Behcets disease
The pathogenesis of Behçet’s disease remains unclear. It might not have a primary autoimmune basis. No specific antibodies or clear-cut abnormalities in B cells have been demonstrated. An infectious trigger in a genetically predisposed host is postulated.
Heat shock protein release interacting with Toll-like receptors causing release of cytokines such as IL-1, IL-8, IL-12, and IL-17, which leads to neutrophil and T helper 1 cell hyperactivity, has been reported in patients with Behçet’s disease. Some investigators think Behçet’s may be an autoinflammatory disorder; however, the rarity of fever during flares, the lack of a defined genetic locus, and the older age of onset makes this less likely.
