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Updated: Jul 10, 2026

Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues
Published on: May 8, 2016
Peripheral TNFalpha, but not peripheral IL-1, requires endogenous IL-1 or TNFalpha induction in the brain for the
1Division of Cell Biology, Center for Experimental Medicine, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan.
Abstract:
It is known that peripherally administered IL-1 and TNFalpha induce fever through mechanisms involving prostaglandin (PG)E2. In this report, we compared the signaling cascade induced in the brain by TNFalpha and IL-1. Peripheral administration of TNFalpha-induced enhanced fever in IL-1 Receptor antagonist KO mice, suggesting that IL-1 is involved in the TNFalpha mediated fever. IL-1alpha, but not TNFalpha, induced fever in IL-1alpha/beta/TNFalpha KO mice, although central administration of TNFalpha-induced fever. Only IL-1alpha, but not TNFalpha, induced IL-6 in the IL-1alpha/beta/TNFalpha KO mouse brain, while both cytokines induced cyclooxygenase (Cox)-2. I.c.v. administration of PGE2 induced only transient fever in contrast to the TNFalpha- or IL-1alpha-induced fever that lasted longer. Taken together, either IL-1 or TNFalpha induction in the brain is required for the response induced by TNFalpha but not by IL-1alpha, and that both Cox-2 and IL-6 induction are required for prolonged febrile response against these cytokines.
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