期刊
AUTOIMMUNITY REVIEWS
卷 8, 期 4, 页码 337-342出版社
ELSEVIER
DOI: 10.1016/j.autrev.2008.12.008
关键词
Systemic lupus erythematosus; Epstein-Barr virus; Gene expression; Latency
类别
资金
- NCRR NIH HHS [RR015577, P20 RR020143, RR020143, P20 RR015577, P20 RR015577-059004] Funding Source: Medline
- NIAID NIH HHS [AI31584, AI007633, R37 AI024717, T32 AI007633, R01 AI031584, R01 AI024717] Funding Source: Medline
- NIAMS NIH HHS [AR049084, N01AR12253, AR48940, P30 AR053483-02, P30 AR053483, AR053483, P01 AR049084, P50 AR048940-010004, P50 AR048940, R01 AR042460, AR42460] Funding Source: Medline
Serologic association, cross-reactivity of select EBV-specific antibodies with SLE autoantigens, SLE-like autoimmunity after immunization with EBV peptides, increased EB viral load in SLE patients, and SLE-specific alterations in EBV humoral and cellular immunity implicate Epstein-Barr virus (EBV) in the development of systemic lupus erythematosus (SLE). To investigate SLE-specific differences in EBV gene expression, levels of eight EBV genes were compared between SLE patients and controls by using both ex vivo-infected and un-manipulated peripheral blood mononuclear cells (PBMCs). Expression levels of mRNA were significantly greater by Wilcoxen signed rank test in the ex vivo-infected SLE patient-derived cells for 4 of 8 EBV genes, including BLLF1, 3.2-fold (p<0.004); LMP-2, 1.7-fold (p<0.008); EBNA-1, 1.7-fold (p<0.01): and BcRF1, a proposed DNA binding protein, 1.7-fold (p<0.02). The frequency of LMP-1 gene expression was significantly greater by Chi square analysis in the peripheral blood from SLE patients than controls (44% of patients, 10% of controls p<0.05). PBMCs from SLE patients had greater expression of latent genes as well as increased expression of both latent and lytic genes after infection, suggesting that EBV may participate in SLE etiology through several mechanisms. Such altered infection patterns may contribute to the increased levels of EBV and the molecular mimicry seen in sera from SLE patients. (C) 2008 Elsevier B.V. All rights reserved.
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