Source:http://linkedlifedata.com/resource/pubmed/id/19728295
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
2009-10-26
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pubmed:abstractText |
IL-17 is a proinflammatory cytokine crucial for osteoclastic bone resorption in the presence of osteoblasts or synoviocytes in rheumatoid arthritis. However, the role of IL-17 in osteoclastogenesis from human monocytes alone remains unclear. Here, we investigated the role of IL-17 in osteoclastogenesis from human monocytes alone and the direct effect of infliximab on the osteoclastogenesis induced by IL-17. Human peripheral blood mononuclear cells (PBMC) were cultured for 3 days with M-CSF. After non-adherent cells were removed, IL-17 was added with either infliximab or osteoprotegerin (OPG). Seven days later, adherent cells were stained for vitronectin receptor. On the other hand, CD11b-positive monocytes purified from PBMC were also cultured and stained as described above. CD11b-positive cells were cultured with TNF-alpha and receptor activator of NF-kappaB ligand (RANKL). In the cultures of both adherent cells and CD11b-positive cells, IL-17 dose-dependently induced osteoclastogenesis in the absence of soluble-RANKL. OPG or infliximab inhibited IL-17-induced osteoclastogenesis. Interestingly, in the culture of CD11b-positive cells, the osteoclastogenesis was more potently inhibited by infliximab than by OPG. TNF-alpha and RANKL synergistically induced osteoclastogenesis. The present study clearly demonstrated the novel mechanism by which IL-17 directly induces osteoclastogenesis from human monocytes alone. In addition, infliximab potently inhibits the osteoclastogenesis directly induced by IL-17.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Anti-Inflammatory Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Monoclonal,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD11b,
http://linkedlifedata.com/resource/pubmed/chemical/Integrin alphaVbeta3,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-17,
http://linkedlifedata.com/resource/pubmed/chemical/RANK Ligand,
http://linkedlifedata.com/resource/pubmed/chemical/TNFSF11 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha,
http://linkedlifedata.com/resource/pubmed/chemical/infliximab
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
1097-4644
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pubmed:author | |
pubmed:copyrightInfo |
(c) 2009 Wiley-Liss, Inc.
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pubmed:issnType |
Electronic
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pubmed:day |
1
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pubmed:volume |
108
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
947-55
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pubmed:meshHeading |
pubmed-meshheading:19728295-Animals,
pubmed-meshheading:19728295-Anti-Inflammatory Agents,
pubmed-meshheading:19728295-Antibodies, Monoclonal,
pubmed-meshheading:19728295-Antigens, CD11b,
pubmed-meshheading:19728295-Bone Marrow Cells,
pubmed-meshheading:19728295-Cell Adhesion,
pubmed-meshheading:19728295-Humans,
pubmed-meshheading:19728295-Integrin alphaVbeta3,
pubmed-meshheading:19728295-Interleukin-17,
pubmed-meshheading:19728295-Leukocytes, Mononuclear,
pubmed-meshheading:19728295-Macrophages,
pubmed-meshheading:19728295-Male,
pubmed-meshheading:19728295-Mice,
pubmed-meshheading:19728295-Monocytes,
pubmed-meshheading:19728295-Osteoblasts,
pubmed-meshheading:19728295-Osteoclasts,
pubmed-meshheading:19728295-RANK Ligand,
pubmed-meshheading:19728295-Tumor Necrosis Factor-alpha
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pubmed:year |
2009
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pubmed:articleTitle |
IL-17 induces osteoclastogenesis from human monocytes alone in the absence of osteoblasts, which is potently inhibited by anti-TNF-alpha antibody: a novel mechanism of osteoclastogenesis by IL-17.
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pubmed:affiliation |
Institute of Rheumatology, Tokyo Women's Medical University, 10-22 Kawada-cho, Shinjuku-ku, Tokyo 162-0054, Japan. toruyago@ior.twmu.ac.jp
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pubmed:publicationType |
Journal Article
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