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Immunology and inflammation
Reduced response to Epstein–Barr virus antigens by T-cells in systemic lupus erythematosus patients
  1. Anette Holck Draborg1,
  2. Søren Jacobsen2,
  3. Marie Westergaard1,
  4. Shila Mortensen3,
  5. Janni Lisander Larsen2,
  6. Gunnar Houen1 and
  7. Karen Duus1
  1. 1Department of Clinical Biochemistry, Immunology and Genetics, Statens Serum Institut, Copenhagen, Denmark
  2. 2Department of Infectious Diseases and Rheumatology, Rigshospitalet, Copenhagen University Hospital, Copenhagen, Denmark
  3. 3Department of Microbiological Diagnostics and Virology, Statens Serum Institut, Copenhagen, Denmark
  1. Correspondence to Professor Gunnar Houen; gh{at}ssi.dk

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.

  • Systemic lupus erythematosus
  • Epstein-Barr virus
  • T-cells
  • antibodies

This is an Open Access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 3.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/3.0/

https://doi.org/10.1136/lupus-2014-000015

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