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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
1996-10-25
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pubmed:abstractText |
Chronic immune responses and inflammatory reactions in rheumatoid arthritis (RA) often cause severe destruction of cartilage and bone, but its mechanism is still a matter of controversy. We reported that interleukin-6 (IL-6) alone does not induce osteoclast formation, but soluble interleukin-6 receptors (sIL-6R) triggered the formation in the presence of IL-6 in cocultures of murine osteoblastic cells and bone marrow cells. In this study, we examined the involvement of sIL-6R and IL-6 in joint destruction in patients with RA. Although the frequency of patients having osteoclast-like multinucleated cells in synovium derived from the knee joint was not significantly different between RA (65%) and osteoarthritis (OA) patients (43%), the number of osteoclast-like cells found in the synovium was greater in the former than in the latter. Multinucleated cells obtained from RA synovium expressed the osteoclast-specific phenotype such as tartrate-resistant acid phosphatase, carbonic anhydrase II, vacuolar proton-ATPase and vitronectin receptors at similar levels to those from a human giant cell tumor of bone. The concentration of both IL-6 and sIL-6R was significantly higher in the synovial fluids from patients with RA than with OA. The concentration of IL-6 and sIL-6R correlated well with the roentgenologic grades of joint destruction. Dose-response curves for human IL-6 and human sIL-6R in inducing osteoclast-like cell formation in cocultures indicated that the RA synovial fluids contained sufficient IL-6 and sIL-6R to induce osteoclastogenesis. When synovial fluids from RA and OA patients were added to the cocultures, some of the RA synovial fluids containing high levels of IL-6 and sIL-6R stimulated osteoclast-like cell formation, which was strikingly inhibited by adding anti-IL-6R antibody simultaneously. These results suggest that IL-6 in the RA synovial fluids is at least in part responsible for joint destruction in the presence of sIL-6R through osteoclastogenesis.
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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/Acid Phosphatase,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-6,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-6
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0884-0431
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
11
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
88-95
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:8770701-Acid Phosphatase,
pubmed-meshheading:8770701-Adult,
pubmed-meshheading:8770701-Aged,
pubmed-meshheading:8770701-Aged, 80 and over,
pubmed-meshheading:8770701-Animals,
pubmed-meshheading:8770701-Antigens, CD,
pubmed-meshheading:8770701-Arthritis, Rheumatoid,
pubmed-meshheading:8770701-Cells, Cultured,
pubmed-meshheading:8770701-Female,
pubmed-meshheading:8770701-Humans,
pubmed-meshheading:8770701-Interleukin-6,
pubmed-meshheading:8770701-Male,
pubmed-meshheading:8770701-Mice,
pubmed-meshheading:8770701-Middle Aged,
pubmed-meshheading:8770701-Osteoarthritis,
pubmed-meshheading:8770701-Osteoblasts,
pubmed-meshheading:8770701-Osteoclasts,
pubmed-meshheading:8770701-Phenotype,
pubmed-meshheading:8770701-Receptors, Interleukin,
pubmed-meshheading:8770701-Receptors, Interleukin-6,
pubmed-meshheading:8770701-Solubility,
pubmed-meshheading:8770701-Synovial Fluid,
pubmed-meshheading:8770701-Synovial Membrane
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pubmed:year |
1996
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pubmed:articleTitle |
Interleukin-6 and soluble interleukin-6 receptors in the synovial fluids from rheumatoid arthritis patients are responsible for osteoclast-like cell formation.
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pubmed:affiliation |
Institute of Rheumatology, Tokyo Women's Medical College, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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