Source:http://linkedlifedata.com/resource/pubmed/id/10201961
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
7
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pubmed:dateCreated |
1999-5-13
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pubmed:abstractText |
T lymphocytes are a major component of the inflammatory infiltrate in rheumatoid synovitis, but their exact role in the disease process is not understood. Functional activities of synovial T cells were examined by adoptive transfer experiments in human synovium-SCID mouse chimeras. Adoptive transfer of tissue-derived autologous CD8+ T cells induced a marked reduction in the activity of lesional T cells and macrophages. Injection of CD8+, but not CD4+, T cells decreased the production of tissue IFN-gamma, IL-1beta, and TNF-alpha by >90%. The down-regulatory effect of adoptively transferred CD8+ T cells was not associated with depletion of synovial CD3+ T cells or synovial CD68+ macrophages, and it could be blocked by Abs against IL-16, a CD8+ T cell-derived cytokine. In the synovial tissue, CD8+ T cells were the major source of IL-16, a natural ligand of the CD4 molecule that can anergize CD4-expressing cells. The anti-inflammatory activity of IL-16 in rheumatoid synovitis was confirmed by treating synovium-SCID mouse chimeras with IL-16. Therapy for 14 days with recombinant human IL-16 significantly inhibited the production of IFN-gamma, IL-1beta, and TNF-alpha in the synovium. We propose that tissue-infiltrating CD8+ T cells in rheumatoid synovitis have anti-inflammatory activity that is at least partially mediated by the release of IL-16. Spontaneous production of IL-16 in synovial lesions impairs the functional activity of CD4+ T cells but is insufficient to completely abrogate their stimulation. Supplemental therapy with IL-16 may be a novel and effective treatment for rheumatoid arthritis.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
162
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
4293-9
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:10201961-Animals,
pubmed-meshheading:10201961-Anti-Inflammatory Agents, Non-Steroidal,
pubmed-meshheading:10201961-Arthritis, Rheumatoid,
pubmed-meshheading:10201961-CD8-Positive T-Lymphocytes,
pubmed-meshheading:10201961-Cells, Cultured,
pubmed-meshheading:10201961-Chronic Disease,
pubmed-meshheading:10201961-Down-Regulation,
pubmed-meshheading:10201961-Humans,
pubmed-meshheading:10201961-Injections, Intraperitoneal,
pubmed-meshheading:10201961-Interleukin-16,
pubmed-meshheading:10201961-Mice,
pubmed-meshheading:10201961-Mice, Inbred NOD,
pubmed-meshheading:10201961-Mice, SCID,
pubmed-meshheading:10201961-Synovial Membrane,
pubmed-meshheading:10201961-Synovitis
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pubmed:year |
1999
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pubmed:articleTitle |
IL-16 as an anti-inflammatory cytokine in rheumatoid synovitis.
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pubmed:affiliation |
Department of Medicine, Division of Rheumatology, Mayo Clinic and Foundation, Rochester, MN 55905, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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