Source:http://linkedlifedata.com/resource/pubmed/id/14707107
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
|
| pubmed:dateCreated |
2004-1-6
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| pubmed:abstractText |
EBV infection is more common in patients with systemic lupus erythematosus (SLE) than in control subjects, suggesting that this virus plays an etiologic role in disease and/or that patients with lupus have impaired EBV-specific immune responses. In the current report we assessed immune responsiveness to EBV in patients with SLE and healthy controls, determining virus-specific T cell responses and EBV viral loads using whole blood recall assays, HLA-A2 tetramers, and real-time quantitative PCR. Patients with SLE had an approximately 40-fold increase in EBV viral loads compared with controls, a finding not explained by disease activity or immunosuppressive medications. The frequency of EBV-specific CD69+ CD4+ T cells producing IFN-gamma was higher in patients with SLE than in controls. By contrast, the frequency of EBV-specific CD69+ CD8+ T cells producing IFN-gamma in patients with SLE appeared lower than that in healthy controls, although this difference was not statistically significant. These findings suggest a role for CD4+ T cells in controlling, and a possible defect in CD8+ T cells in regulating, increased viral loads in lupus. These ideas were supported by correlations between viral loads and EBV-specific T cell responses in lupus patients. EBV viral loads were inversely correlated with the frequency of EBV-specific CD69+ CD4+ T cells producing IFN-gamma and were positively correlated with the frequencies of CD69+ CD8+ T cells producing IFN-gamma and with EBV-specific, HLA-A2 tetramer-positive CD8+ T cells. These results demonstrate that patients with SLE have defective control of latent EBV infection that probably stems from altered T cell responses against EBV.
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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
|
| pubmed:month |
Jan
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| pubmed:issn |
0022-1767
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| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
15
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| pubmed:volume |
172
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| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
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| pubmed:pagination |
1287-94
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| pubmed:dateRevised |
2007-11-14
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| pubmed:meshHeading |
pubmed-meshheading:14707107-Adult,
pubmed-meshheading:14707107-B-Lymphocyte Subsets,
pubmed-meshheading:14707107-CD4-Positive T-Lymphocytes,
pubmed-meshheading:14707107-CD8-Positive T-Lymphocytes,
pubmed-meshheading:14707107-Cytomegalovirus,
pubmed-meshheading:14707107-Epitopes, T-Lymphocyte,
pubmed-meshheading:14707107-Epstein-Barr Virus Infections,
pubmed-meshheading:14707107-Female,
pubmed-meshheading:14707107-Herpesvirus 4, Human,
pubmed-meshheading:14707107-Humans,
pubmed-meshheading:14707107-Leukocytes, Mononuclear,
pubmed-meshheading:14707107-Lupus Erythematosus, Systemic,
pubmed-meshheading:14707107-Lymphocyte Count,
pubmed-meshheading:14707107-Male,
pubmed-meshheading:14707107-Middle Aged,
pubmed-meshheading:14707107-Severity of Illness Index,
pubmed-meshheading:14707107-Viral Load,
pubmed-meshheading:14707107-Virus Latency
|
| pubmed:year |
2004
|
| pubmed:articleTitle |
Defective control of latent Epstein-Barr virus infection in systemic lupus erythematosus.
|
| pubmed:affiliation |
Section of Rheumatology, Department of Internal Medicine, Yale University School of Medicine, 300 Cedar Street, New Haven, CT 06520, 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
|