Since cytokines have such potent effects, it is clearly important that their action be limited to avoid the pathogenic effects of cytokine overdose. This subject is only beginning to be understood. For II.-1 there is a receptor antagonist which interferes with II.-1 binding to its receptors, but by far the most common inhibitors of cytokines appear to be truncated forms of the extracellular domain of the receptors. Such molecules have been demonstrated for II.-1 (type II), 1L-2 (p55), IL-4, IL-7, TNF-R (both chains) and IFN-y, and are not limited to cytokines; similar molecules are also found for hormones, e.g. growth hormone receptor and IGF-1 receptor and adhesion molecules. There is also a soluble extracellular domain of the IL-6 receptor, but it is costimulatorv as opposed to inhibitory. The current concept is that circulating cytokine inhibitors prevent small concentrations of cytokines from exerting prolonged or diffuse effects. It is likely that the balance of cyto-kine-to-cytokine inhibitor will be of paramount importance in determining whether cytokines exert physiological or pathological effects. There is now clear-cut evidence that excess TNFa signaling is involved in the pathogenesis of rheumatoid arthritis.
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