The inhibition of the proinflammatory cytokine tumor necrosis factor a (TNF-α) is considered an essential factor in the treatment of diseases as diverse as multiple sclerosis, rheumatoid arthritis, Crohn disease, systemic lupus erythematosus, and some forms of diabetes, as well as other diseases that involve selective immunologic attack on a particular organ or system.1 In autoimmune disease, interleukin-1 (IL-1) acts by stimulating other cells to produce cytokines or enzymes that then act on the target tissue.2 In addition, TNF-α can stimulate the production of IL-1; hence, both molecules are likely to be involved in the pathogenesis of septic shock and other diseases. The cytokines IL-1β and TNF-α are often grouped together and called proinflammatory cytokines. The biochemical changes induced by TNF-α and IL-1β include increased synthesis of nitric oxide and endothelial cell adhesion molecules. Once TNF-α and IL-1β are secreted, the cascade of inflammation erupts with secondary secretion
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