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- W2055272095 abstract "Abstract It is widely believed that IL‐4 exerts its influence by profiling the immune response during priming and expansion of immune cells, and thereby modulates the outcome of chronic inflammation. In the present investigation, collagen antibody‐induced arthritis (CAIA) was used to delineate the role of IL‐4 in a T cell‐independent inflammatory phase. Mice predisposed to Th2 cytokines (BALB/c and STAT4‐deficient mice) developed a more severe arthritis than mice biased towards Th1 cytokines (C57BL/6 and STAT6‐deficient mice). Reduced incidence of CAIA was observed in IL‐4‐deficient mice compared to control littermates. Infiltrating cells in the paws of IL‐4‐sufficient mice had increased osteoclast activity and tumor necrosis factor (TNF)‐α and interleukin (IL)‐1β secretion. Massive infiltration of granulocytes and joint and cartilage damage were present in arthritic paws. Depletion of IL‐4 suppressed CAIA, which was abrogated by IFN‐γ neutralization. IL‐1R‐ and IL‐1RTNFR‐deficient mice were completely resistant to CAIA. Thus, IL‐4 promotes an antibody‐mediated and TNF‐α/IL‐1β‐dependent inflammation in vivo ." @default.
- W2055272095 created "2016-06-24" @default.
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- W2055272095 date "2006-05-24" @default.
- W2055272095 modified "2023-10-15" @default.
- W2055272095 title "Arthritis induced with cartilage-specific antibodiesis IL-4-dependent" @default.
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- W2055272095 doi "https://doi.org/10.1002/eji.200535633" @default.
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