rdf:type |
|
lifeskim:mentions |
|
pubmed:issue |
49
|
pubmed:dateCreated |
2004-12-8
|
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.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/15569925-10395323,
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pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:month |
Dec
|
pubmed:issn |
0027-8424
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pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:day |
7
|
pubmed:volume |
101
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
17180-5
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:15569925-Adipokines,
pubmed-meshheading:15569925-Adult,
pubmed-meshheading:15569925-Aged,
pubmed-meshheading:15569925-Arthritis, Rheumatoid,
pubmed-meshheading:15569925-Autoantigens,
pubmed-meshheading:15569925-CD4-Positive T-Lymphocytes,
pubmed-meshheading:15569925-Case-Control Studies,
pubmed-meshheading:15569925-Cell Communication,
pubmed-meshheading:15569925-Female,
pubmed-meshheading:15569925-Glycoproteins,
pubmed-meshheading:15569925-Humans,
pubmed-meshheading:15569925-Immunity, Cellular,
pubmed-meshheading:15569925-Inflammation,
pubmed-meshheading:15569925-Lectins,
pubmed-meshheading:15569925-Male,
pubmed-meshheading:15569925-Middle Aged,
pubmed-meshheading:15569925-Th1 Cells
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pubmed:year |
2004
|
pubmed:articleTitle |
Functional regulatory immune responses against human cartilage glycoprotein-39 in health vs. proinflammatory responses in rheumatoid arthritis.
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pubmed:affiliation |
Departments of Rheumatology, Leiden University Medical Center, P.O. Box 9600, 2300 RC Leiden, The Netherlands.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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