pubmed-article:10201961 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:10201961 | lifeskim:mentions | umls-concept:C0065337 | lld:lifeskim |
pubmed-article:10201961 | lifeskim:mentions | umls-concept:C0039103 | lld:lifeskim |
pubmed-article:10201961 | lifeskim:mentions | umls-concept:C0003209 | lld:lifeskim |
pubmed-article:10201961 | lifeskim:mentions | umls-concept:C0079189 | lld:lifeskim |
pubmed-article:10201961 | lifeskim:mentions | umls-concept:C1515999 | lld:lifeskim |
pubmed-article:10201961 | pubmed:issue | 7 | lld:pubmed |
pubmed-article:10201961 | pubmed:dateCreated | 1999-5-13 | lld:pubmed |
pubmed-article:10201961 | 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. | lld:pubmed |
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pubmed-article:10201961 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10201961 | pubmed:language | eng | lld:pubmed |
pubmed-article:10201961 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10201961 | pubmed:citationSubset | AIM | lld:pubmed |
pubmed-article:10201961 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10201961 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10201961 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:10201961 | pubmed:month | Apr | lld:pubmed |
pubmed-article:10201961 | pubmed:issn | 0022-1767 | lld:pubmed |
pubmed-article:10201961 | pubmed:author | pubmed-author:KlimiukP APA | lld:pubmed |
pubmed-article:10201961 | pubmed:author | pubmed-author:WeyandC MCM | lld:pubmed |
pubmed-article:10201961 | pubmed:author | pubmed-author:GoronzyJ JJJ | lld:pubmed |
pubmed-article:10201961 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:10201961 | pubmed:day | 1 | lld:pubmed |
pubmed-article:10201961 | pubmed:volume | 162 | lld:pubmed |
pubmed-article:10201961 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:10201961 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:10201961 | pubmed:pagination | 4293-9 | lld:pubmed |
pubmed-article:10201961 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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pubmed-article:10201961 | pubmed:year | 1999 | lld:pubmed |
pubmed-article:10201961 | pubmed:articleTitle | IL-16 as an anti-inflammatory cytokine in rheumatoid synovitis. | lld:pubmed |
pubmed-article:10201961 | pubmed:affiliation | Department of Medicine, Division of Rheumatology, Mayo Clinic and Foundation, Rochester, MN 55905, USA. | lld:pubmed |
pubmed-article:10201961 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:10201961 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:10201961 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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