IL-1F5 mediates anti-inflammatory activity in the brain through induction of IL-4 following interaction with SIGIRR/TIR8

摘要: Similarity in structure and sequence homology has led to the identification of new members interleukin-1 (IL-1) ligand receptor superfamilies. IL-1F6, IL-1F8 IL-1F9 have been shown signal through IL-1R-related protein 2 IL-1 accessory leading activation NFκB, while IL-1F7 IL-1F10 interact with IL-18 soluble type I respectively. In contrast, a biological role for IL-1F5 remained elusive, conflicting data relating its possible ability antagonize IL-1F9-stimulated NFκB Jurkat cells transfected 2. this study, we set out investigate brain report that it antagonizes inflammatory effects IL-1β lipopolysaccharide (LPS) vivo vitro including inhibitory effect on long-term potentiation (LTP) rat hippocampus. We demonstrate induces IL-4 mRNA expression glia enhances hippocampal following intracerebroventricular (i.c.v.) injection. The LPS-induced is attenuated from IL-4-defective (IL−4−/− mice). Our findings suggest mediates anti-inflammatory induce production consequence interaction orphan receptor, single Ig molecule (SIGIRR)/TIR8, as were not observed SIGIRR−/− mice. contrast tissue, did attenuate changes, or up-regulated macrophages dendritic cells, suggesting confined brain.