Research continues to unravel the details of the pathogenesis of inflammatory disorders, participates in many of these conditions as a proinflammatory cytokine, very "upstream" in the inflammatory process, responsible for the recruitment of other proinflammatory cytokines such as IL-1, as well as the stimulation of factors responsible for attraction of inflammatory cells, synthesis of acute phase proteins, angiogenesis, and metalloproteinase enzyme synthesis. In some cases works together with other cytokines to drive the inflammatory process. Inhibition of this key mediator has been demonstrated to have a potent anti-inflammatory effect in several models. The role of this cytokine in the pathogenesis of osteoporosis and loss of bone in inflammatory conditions is currently under intense investigation.
While TNFa is undoubtedly a major player in inflammation, it would be naive to believe that this complex process can be controlled completely in all of our patients through the inhibition of this single molecule. There are patients whose inflammatory disease seems resistant to blockade. The possibility of disease subsets, each driven by specific dominant cytokines or combinations of cytokines in an attractive hypothesis. The important role of other cytokines such as IL-1, IL-15, IL-17, and others can be demonstrated in conditions of inflammation. Combination cytokine inhibition is a strategy just now being tested in the clinical setting.
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