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作 者:Jennifer L.Horton Elena B.Samoilova Thomas A.Judge Laurence A.Turka James M.Wilson
机构地区:[1]Department of Molecular and Cellular Engineering,Department of Medicine,University of Pennsylvania School of Medicine,Philadelphia,PA 19104,Department of Medicine,University of Pennsylvania School of Medicine,Philadelphia,PA 19104,Department of Medicine,University of Pennsylvania School of Medicine,Philadelphia,PA 19104,Department of Molecular and Cellular Engineering [2]Department of Medicine,University of pennsylvania School of Medicine,Philadelphia,PA 19104
出 处:《中国实验血液学杂志》1997年第3期322-322,共1页Journal of Experimental Hematology
摘 要:Both rheumatoid arthritis and animal models ofautoimmune arthritis are characterized by hyper-activation of synovial cells and hyperplasia of the synovialmembrane. The activated synovial cells produceinflammatory cytokines and degradative enzymes whichlead to destruction of cartilage and bones. Effectivetreatment of arthritis may require elimination of most orall activated synovial cells. The death factor
关 键 词:collagen CARTILAGE DESTRUCTION cytokines bones elimination enzymes AUTOIMMUNE inflammation unlike
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