Interleukin-1 (IL-1) and interferon α (IFNα), cytokines originally detected in immunological cells, now have been shown to produce nonimmunological host defense responses of central and peripheral origins. These cytokines are released from glial cells in the brain in pathological states. Local application of IL-1β and IFNα to thermosensitive neurons in the preoptic and anterior hypothalamus and glucose responsive neurons in the ventromedial hypothalamus in vivo and in vitro, altered the activity in appropriate ways to explain the cytokines-induced fever and anorexia, respectively. The responses to IL-1β, but not to IFNα, were blocked by sodium salicylate, suggesting the involvement of synthesis of prostaglandins, αMSH, an endogenous antipyretic and a possible antagonist of IL-1β at lymphocytes, specifically depressed the responses to IL-1β, but not those to IFNα. In contrast, the action of IFNα was reversibly blocked by naloxone, suggesting the opioid receptor mediation. Intracerebral injection of IFNα and β-endorphin in the rat and mouse resulted in the suppression of cytotoxic activity of natural killer cells in the spleen by activation of brain opioid receptor, which was shown to be mediated predominantly by splenic sympathetic nerves. The results suggest a view that immune cytokines may provide afferent links for the regulatory circuits between the brain and the immune system.
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