期刊
JOURNAL OF IMMUNOLOGY
卷 172, 期 2, 页码 1287-1294出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.172.2.1287
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- NIAMS NIH HHS [AR 44076, AR 40072] Funding Source: Medline
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 similar to40-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. The Journal of Immunology, 2004, 172: 1287-1294.
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