Reduced response to Epstein–Barr virus antigens by T-cells in systemic lupus erythematosus patients

Abstract

ObjectiveEpstein–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.MethodsT cells were analyzed by flow cytometry and antibodies were analyzed by enzyme-linked immunosorbent assay.ResultsSLE 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.ConclusionsThese 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.

The phenolic fraction of extra virgin olive oil modulates the activation and the inflammatory response of T cells from patients with systemic lupus erythematosus and healthy donors

“…Besides, T‐cell activation is a fundamental step for the onset of the adaptive immune response. In this regard, CD69 is thought to be among the earliest surface markers of T‐cell activation, and its changes are correlated with SLE disease activity . In fact, active SLE patients show increased CD69 expression levels in comparison with inactive patients and healthy subjects .…”

Isotypes of Epstein-Barr Virus Antibodies in Rheumatoid Arthritis: Association with Rheumatoid Factors and Citrulline-Dependent Antibodies

“…Clinical characteristics of all patients and controls are outlined in Table 1 . SLE patients and HCs have previously been reported on in the study by Draborg et al [ 17 ] as well as RA patients in the study by Troelsen et al [ 18 ].…”

Epstein-Barr Virus (EBV) Encoded Dutpase Exacerbates the Immune pathology of Lupus Nephritis In Vivo

“…These studies demonstrated that the EBV-dUTPase: (i) induce the secretion of the pro-inflammatory T H 1/T H 17 cytokines IL-6, IL-1β and type-I IFN in a TLR2dependent manner [17,18,21], (ii) up-regulates the expression of the inflammatory BIC/microRNA-155 [18], and (iii) alters EBV-specific CD8+ T-cell function by up-regulating the expression of several genes involved with the antiviral immune response [18]. These findings have also been reported in patients with SLE [13][14][15]22]. The data presented in this study demonstrate that the EBV-dUTPase may play a role in the immune over-reactivity observed in a subset of patients with LN by triggering abnormal innate and adaptive immune responses thus, inducing an immune amplification cascade that promotes autoimmunity.…”

“…Other studies demonstrated that antibodies directed against Epstein-Barr nuclear antigen 1 (EBNA-1) cross react with autoantigens associated with SLE [11] as well as dsDNA [12]. Furthermore, an increased EBV viral load in SLE patients was also demonstrated [13][14][15]. Whether or not the increased viral titers and EBV-specific immune responses observed in SLE reflect the sensitivity of the virus to perturbations in the immune system in these patients [16], and thus, represent a consequence of SLE rather than its cause, remains a topic of controversy.…”