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The pathogenesis of vasculitis is complex and it involves multiple mechanisms. The proposed mechanisms include: (1) pathogenic immune complex formation and deposition in the vessel walls; (2) autoantibodies such as antineutrophil cytoplasmic antibodies and antiendothelial cell antibodies; (3) cellular and molecular immune responses involving cytokines and adhesion molecules; (4) granuloma formation; and (5) damaged or altered endothelial cell function due to infectious organisms, tumors, or toxins. Cytokines are small proteins or glycoproteins that are secreted for the purpose of altering the function of target cells in an endocrine (uncommon), paracrine, or autocrine fashion, and they are produced by cells acting individually (e.g., lymphocytes or macrophages) or as components of a tissue (e.g., intestinal epithelium). Takayasu arteritis, vascular Bechet disease and Buerger’s disease are classified as large and medium size vasculitis, and autoimmunity is known to be their pathogenesis. The mediators of cellular immunity, the cytokines, may be involved in a variety of vasculitis conditions. Some authors have reported that Interleukin-1 and 6, and RANTES (Regulated on Activation, Normal T-cell Expressed and Secreted) are the major cytokines in Takayasu arteritis, and Th1 cytokine is the major cytokine in Bechet disease. The role of these cytokines in the pathogenesis of the each vasculitis is still a matter of debate, but these cytokines have partial, specific roles in the initiation and progress of vascultitis. The particular pattern of cytokine changes is associated with vasculitis, and cytokines should be considered for monitoring the disease activity and therapy.
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