Source:http://linkedlifedata.com/resource/pubmed/id/14726963
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
6
|
| pubmed:dateCreated |
2004-1-16
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| pubmed:abstractText |
High levels of soluble CD30 (sCD30) were detected in the serum and synovial fluid of patients with rheumatoid arthritis (RA), indicating the involvement of CD30+ T cells in the pathogenesis. We investigated the induction of CD30 and its functions in CD4+T cells from patients with established RA (disease duration >_2 years). CD4+ T cells from both the peripheral blood (PB) and synovial tissue (ST) of RA patients expressed surface CD30 when stimulated with anti-CD3 antibody (Ab) and anti-CD28 Ab, but their CD30 induction was slower and weaker compared with PB CD4+ T cells of healthy controls (HC). Immunohistochemical analysis showed that only a small proportion of lymphocytes expressed CD30 in the ST (-1%). RA PB CD4+ T cells, after recovery from 6-day stimulation with anti-CD3 Ab and anti-CD28 Ab, showed in intracellular cytokine staining that CD30+ T cells could produce more interleukin-4 (IL-4) but less interferon-gamma. In the culture of RA PB CD4+ T Cells with anti-CD3 Ab and anti-CD28 Ab, blocking anti-CD30 Ab similarly inhibited the cell proliferation and activation of nuclear factor-kappaB on day 4 in RA and HC, but inhibited the apoptotic cell death on day 6 only in RA. These results indicate that despite high-level expression of sCD30, the anti-inflammatory activity of IL-4-producing CD30+ CD4+ T cells may be limited in the ST due to a poor induction of surface CD30 and a susceptibility to CD30-mediated cell death.
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| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Dec
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| pubmed:issn |
0386-300X
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
57
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| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
267-77
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| pubmed:dateRevised |
2006-11-15
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| pubmed:meshHeading |
pubmed-meshheading:14726963-Adult,
pubmed-meshheading:14726963-Aged,
pubmed-meshheading:14726963-Aged, 80 and over,
pubmed-meshheading:14726963-Antigens, CD30,
pubmed-meshheading:14726963-Antigens, CD4,
pubmed-meshheading:14726963-Apoptosis,
pubmed-meshheading:14726963-Arthritis, Rheumatoid,
pubmed-meshheading:14726963-CD4-Positive T-Lymphocytes,
pubmed-meshheading:14726963-Cell Division,
pubmed-meshheading:14726963-Female,
pubmed-meshheading:14726963-Gene Expression,
pubmed-meshheading:14726963-Humans,
pubmed-meshheading:14726963-Interleukin-4,
pubmed-meshheading:14726963-Male,
pubmed-meshheading:14726963-Middle Aged,
pubmed-meshheading:14726963-NF-kappa B,
pubmed-meshheading:14726963-Signal Transduction,
pubmed-meshheading:14726963-Solubility,
pubmed-meshheading:14726963-Synovial Membrane
|
| pubmed:year |
2003
|
| pubmed:articleTitle |
Pathophysiological functions of CD30+ CD4+ T cells in rheumatoid arthritis.
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| pubmed:affiliation |
Department of Medicine and Clinical Science, Okayama University Graduate School of Medicine and Dentistry, Okayama 700-8558, Japan.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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