Reduced response to Epstein–Barr virus antigens by T-cells in systemic lupus erythematosus patients. Issue 1 (3rd April 2014)

• Record Type: Journal Article
• Authors: Draborg, Anette Holck; Jacobsen, Søren; Westergaard, Marie; Mortensen, Shila; Larsen, Janni Lisander; Houen, Gunnar; Duus, Karen
• Is Part Of: Lupus science & medicine. Volume 1:Issue 1(2014)
• Publication Date: 2014-04-03
• Subjects: Systemic lupus erythematosus -- Epstein-Barr virus -- T-cells -- antibodies; Systemic lupus erythematosus -- Periodicals; 616.772005
• DOI: 10.1136/lupus-2014-000015
• Languages: English
• ISSNs: 2398-8851

Abstract

Abstract : Objective: Epstein–Barr virus (EBV) has for long been associated with systemic lupus erythematosus (SLE). In this study, we investigated the levels of latent and lytic antigen EBV-specific T-cells and antibodies in SLE patients. Methods: T cells were analyzed by flow cytometry and antibodies were analyzed by enzyme-linked immunosorbent assay. Results: SLE patients showed a significantly reduced number of activated (CD69) T-cells upon ex vivo stimulation with EBV nuclear antigen (EBNA) 1 or EBV early antigen diffuse (EBV-EA/D) in whole blood samples compared with healthy controls. Also, a reduced number of T-cells from SLE patients were found to produce interferon-γ upon stimulation with these antigens. Importantly, responses to a superantigen were normal in SLE patients. Compared with healthy controls, SLE patients had fewer EBV-specific T-cells but higher titres of antibodies against EBV. Furthermore, an inverse correlation was revealed between the number of lytic antigen EBV-specific T-cells and disease activity of the SLE patients, with high-activity SLE patients having fewer T-cells than low-activity SLE patients. Conclusions: These results indicate a limited or a defective EBV-specific T-cell response in SLE patients, which may suggest poor control of EBV infection in SLE with an immune reaction shift towards a humoral response in an attempt to control viral reactivation. A role for decreased control of EBV as a contributing agent in the development or exacerbation of SLE is proposed.