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• W2897600982 abstract "Abstract Auto-inflammatory syndrome, a condition clinically distinct from rheumatoid arthritis, is characterized by systemic inflammation in tissues such as major joints, skin, and internal organs. Autonomous innate-immune activation is thought to promote this inflammation, but underlying pathological mechanisms have not been clarified nor are treatment strategies established. Here, we newly established a mouse model in which IL-1 signaling is conditionally activated in adult mice (hIL-1 cTg) and observed phenotypes similar to those seen in auto-inflammatory syndrome patients. In serum of hIL-1 cTg mice, IL-6 and IL-17 levels significantly increased, and signal transducer and activator of transcription 3 (Stat3) was activated in joints. When we crossed hIL-1 cTg with either IL-6- or IL-17-deficient mice or with Stat3 conditional knockout mice, phenotypes seen in hIL-1 cTg mice were significantly ameliorated. Thus, IL-6, IL-17 and Stat3 all represent potential therapeutic targets for this syndrome." @default.
• W2897600982 created "2018-10-26" @default.
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• W2897600982 date "2018-10-25" @default.
• W2897600982 modified "2023-10-16" @default.
• W2897600982 title "IL-6, IL-17 and Stat3 are required for auto-inflammatory syndrome development in mouse" @default.
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• W2897600982 doi "https://doi.org/10.1038/s41598-018-34173-5" @default.
• W2897600982 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6202393" @default.
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• W2897600982 hasPublicationYear "2018" @default.
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