pubmed-article:15569925 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:15569925 | lifeskim:mentions | umls-concept:C0003873 | lld:lifeskim |
pubmed-article:15569925 | lifeskim:mentions | umls-concept:C0205245 | lld:lifeskim |
pubmed-article:15569925 | lifeskim:mentions | umls-concept:C0018684 | lld:lifeskim |
pubmed-article:15569925 | lifeskim:mentions | umls-concept:C1704632 | lld:lifeskim |
pubmed-article:15569925 | lifeskim:mentions | umls-concept:C0871261 | lld:lifeskim |
pubmed-article:15569925 | lifeskim:mentions | umls-concept:C0301872 | lld:lifeskim |
pubmed-article:15569925 | lifeskim:mentions | umls-concept:C0528649 | lld:lifeskim |
pubmed-article:15569925 | lifeskim:mentions | umls-concept:C2911692 | lld:lifeskim |
pubmed-article:15569925 | lifeskim:mentions | umls-concept:C1706817 | lld:lifeskim |
pubmed-article:15569925 | lifeskim:mentions | umls-concept:C0220905 | lld:lifeskim |
pubmed-article:15569925 | pubmed:issue | 49 | lld:pubmed |
pubmed-article:15569925 | pubmed:dateCreated | 2004-12-8 | lld:pubmed |
pubmed-article:15569925 | pubmed:abstractText | The class of immune response against autoantigens could profoundly influence the onset and/or outcome of autoimmune diseases. Until now, there is only limited information on the antigen-specific balance between proinflammatory and regulatory responses in humans. Here we analyzed the natural immune response against a candidate autoantigen in rheumatoid arthritis, human cartilage glycoprotein-39 (HC gp-39). Peripheral blood mononuclear cells from healthy individuals reacted against HC gp-39 with the production of IL-10 but not IFN-gamma. Ex vivo assays indicated that the naturally occurring HC gp-39-specific immune response in bulk is powerful enough to suppress antigen-specific recall responses, demonstrating that rather than being unresponsive, the HC gp-39-directed immune response in healthy individuals shows a strong bias toward a regulatory phenotype. Moreover, CD4(+) T cell lines directed against HC gp-39 expressed CD25, glucocorticoid-induced tumor necrosis factor receptor, and Foxp3 molecules and were capable of suppressing antigen-specific T cell responses. Cell-cell contact was required for this suppression. As opposed to healthy individuals, the HC gp-39-directed immune response in 50% of patients with rheumatoid arthritis exhibits polarization toward a proinflammatory T helper 1 phenotype and is significantly less powerful in suppressing antigen-specific recall responses. Together these findings indicate that the presence of HC gp-39-specific immune responses in healthy individuals may have an inhibitory effect on inflammatory responses in areas where HC gp-39 is present. Furthermore, these data indicate that the class of HC gp-39-directed immune response in rheumatoid arthritis patients has shifted from an antiinflammatory toward a proinflammatory phenotype. | lld:pubmed |
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pubmed-article:15569925 | pubmed:language | eng | lld:pubmed |
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pubmed-article:15569925 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:15569925 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:15569925 | pubmed:month | Dec | lld:pubmed |
pubmed-article:15569925 | pubmed:issn | 0027-8424 | lld:pubmed |
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pubmed-article:15569925 | pubmed:author | pubmed-author:ElferinkDiënn... | lld:pubmed |
pubmed-article:15569925 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:15569925 | pubmed:day | 7 | lld:pubmed |
pubmed-article:15569925 | pubmed:volume | 101 | lld:pubmed |
pubmed-article:15569925 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:15569925 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:15569925 | pubmed:pagination | 17180-5 | lld:pubmed |
pubmed-article:15569925 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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pubmed-article:15569925 | pubmed:year | 2004 | lld:pubmed |
pubmed-article:15569925 | pubmed:articleTitle | Functional regulatory immune responses against human cartilage glycoprotein-39 in health vs. proinflammatory responses in rheumatoid arthritis. | lld:pubmed |
pubmed-article:15569925 | pubmed:affiliation | Departments of Rheumatology, Leiden University Medical Center, P.O. Box 9600, 2300 RC Leiden, The Netherlands. | lld:pubmed |
pubmed-article:15569925 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:15569925 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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