IL-17 promotes bone erosion in murine collagen-induced arthritis through loss of the receptor activator of NF-kappa B ligand/osteoprotegerin balance.
第一作者:
Erik,Lubberts
第一单位:
Rheumatology and Advanced Therapeutics, University Medical Center Nijmegen, Nijmegen, The Netherlands. E.Lubberts@reuma.umcn.nl
作者:
医学主题词
腺病毒, 人(Adenoviruses, Human);动物(Animals);关节炎, 实验性(Arthritis, Experimental);骨和骨组织(Bone and Bones);载体蛋白质类(Carrier Proteins);牛(Cattle);胶原(Collagen);酶联免疫吸附测定(Enzyme-Linked Immunosorbent Assay);基因表达调控(Gene Expression Regulation);基因转移技术(Gene Transfer Techniques);遗传载体(Genetic Vectors);糖蛋白类(Glycoproteins);人类(Humans);注射, 腹腔内(Injections, Intraperitoneal);白细胞介素17(Interleukin-17);配体(Ligands);男(雄)性(Male);膜糖蛋白类(Membrane Glycoproteins);小鼠(Mice);小鼠, 近交DBA(Mice, Inbred DBA);破骨细胞(Osteoclasts);骨保护素(Osteoprotegerin);RANK配体(RANK Ligand);核因子κB受体活化因子(Receptor Activator of Nuclear Factor-kappa B);受体, 胞质和核(Receptors, Cytoplasmic and Nuclear);受体, 肿瘤坏死因子(Receptors, Tumor Necrosis Factor);溶解度(Solubility);滑膜(Synovial Membrane);增量调节(Up-Regulation)
DOI
10.4049/jimmunol.170.5.2655
PMID
12594294
发布时间
2022-03-31
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