ABSTRACT
Interleukin 1, tumor necrosis factor alpha, and interleukin 6 all interact to effect many of the changes in somatic tissue metabolism that characterize the dynamic response to inflammation or injury. Despite evidence that cytokines in some cases contribute to morbidity and even to mortality, there is indisputable evidence that these mediators play a net beneficial role in ensuring host survival in the face of invasive stimuli. Although cytokines have central and pivotal roles in the beneficial host responses to invasive stimuli, an excessive or chronic production of these monokines causes considerable pathology. The evidence that interleukin 1 and tumor necrosis factor are central to the pathogenesis of rheumatoid arthritis is particularly strong. Elevated levels of both cytokines have been recovered from plasma and synovial fluid, and both interleukin 1 and tumor necrosis factor stimulate synovial protease, prostaglandin, and collagenase activity.
