Beh？et's disease (BD) is a multisystemic disease of unknown etiology characterized by chronic relapsing oral-genital ulcers and uveitis. Multiple systemic associations including articular, gastrointestinal, cardiopulmonary, neurologic, and vascular involvement are also observed in BD. Although the etiopathogenesis of the disease remains unknown, increased neutrophil functions such as chemotaxis, phagocytosis, and excessive production of reactive oxygen species (ROS), including superoxide anion, which may be responsible for oxidative tissue damage seen in BD, and also immunological alterations, T lymphocyte abnormalities in both subpopulation and function have been considered to be correlated with the etiopathogenesis of BD. There is some clinical evidence suggesting that emotional stress and hormonal alterations can influence the course and disease activity of BD. 1. Introduction Beh？et’s disease (BD) is a recurrent systemic inflammatory disorder characterized by four major symptoms consisting of oral aphthous ulcers, ocular lesions, skin lesions, and genital ulcerations. Although many studies have been conducted on the etiopathogenesis of the disease, exact mechanisms have not yet been fully understood [1]. Multiple systemic associations including articular, gastrointestinal, cardiopulmonary, neurologic, and vascular involvement are also observed in BD [1, 2]. Although the etiopathogenesis of the disease remains unknown, increased neutrophil functions such as chemotaxis, phagocytosis, and excessive production of reactive oxygen species (ROS), including superoxide anion, which may be responsible for oxidative tissue damage seen in BD, and also immunological alterations, T lymphocyte abnormalities in both subpopulation and function have been considered to be correlated with the etiopathogenesis of BD. It was postulated that Beh？et’s disease is an autoimmune disease. Systemic manifestations such as articular, gastrointestinal, and neurologic manifestations are not associations with the disease. They are different involvements due to the disease [3, 4]. There is also some clinical evidence suggesting that emotional stress and hormonal alterations can influence the course and disease activity of BD [5–7]. 2. Immune System Dysregulations The immunopathogenesis that is currently postulated is shown in Figure 1. Primarily, hypersensitivity of T cells (αβT cells and γδ-T cells) to multiple antigens appears to play a critical role in the pathogenesis. The activation of monocytes subsequent to T-cell activation through CD40–CD154 interactions as well as a variety
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