ArticlePLoS pathogens2011
Exhausted cytotoxic control of Epstein-Barr virus in human lupus.
Article in PLoS pathogens, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers, 1 of them a synthesis that pooled it.
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Who cites it
83 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The risk of systemic lupus erythematosus associated with Epstein-Barr virus infection: a systematic review and meta-analysis.Clinical and experimental medicine · 2019Pooled it
- Comparison of telitacicept and belimumab in systemic lupus erythematosus: a real-word retrospective study.Clinical rheumatology · 2026Article
- Machine learning models identify prognostic factors in systemic lupus erythematosus patients with epstein-barr virus infection.Clinical rheumatology · 2026Article
- Article
- Clinical characteristics and diagnostic indicators of childhood-onset systemic lupus erythematosus complicated with macrophage activation syndrome.Clinical rheumatology · 2026Article
- How Epstein Barr virus shapes lupus autoimmunity: mechanistic insights and therapeutic perspectives.Frontiers in immunology · 2026Review
- Mechanisms of Epstein-Barr virus-associated autoimmunity: a comparative overview.Frontiers in immunology · 2026Review
- Epstein-Barr virus reprograms autoreactive B cells as antigen-presenting cells in systemic lupus erythematosus.Science translational medicine · 2025Article
- Early multiple sclerosis activity associated with TBX21+CD21loCXCR3+ B cell expansion resembling EBV-induced phenotypes.JCI insight · 2025Article
- The PD-1/PD-L1 pathway and Epstein-Barr virus.European journal of medical research · 2025Review
- Type I interferon and mitochondrial dysfunction are associated with dysregulated cytotoxic CD8+ T cell responses in juvenile systemic lupus erythematosus.Clinical and experimental immunology · 2025Article
- Analysis of Key Genes Related to Systemic Lupus Erythematosus and COVID-19.Combinatorial chemistry & high throughput screening · 2025Article
- Epstein-Barr virus as a potentiator of autoimmune diseases.Nature reviews. Rheumatology · 2024Review
- T cell expressions of aberrant gene signatures and Co-inhibitory receptors (Co-IRs) as predictors of renal damage and lupus disease activity.Journal of biomedical science · 2024Article
- An IL-17A-centric response to Epstein-Barr virus DNA mediated by dendritic Cell-T cell interactions.Frontiers in molecular biosciences · 2024Article
- Hypocortisolemic ASIA: a vaccine- and chronic infection-induced syndrome behind the origin of long COVID and myalgic encephalomyelitis.Frontiers in immunology · 2024Review
- Autoimmune Responses and Therapeutic Interventions for Systemic Lupus Erythematosus: A Comprehensive Review.Endocrine, metabolic & immune disorders drug targets · 2024Review
- Elevated Antibody Titers to Epstein-Barr Virus and Cytomegalovirus in Patients with Drug-Induced Lupus.Viruses · 2023Article
- When AHR signaling pathways meet viral infections.Cell communication and signaling : CCS · 2023Review
- Epstein-Barr virus infection as potential indicator of the occurrence and clinical presentation of systemic lupus erythematosus.Frontiers in immunology · 2023Article
23 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Systemic Lupus Erythematosus (SLE) pathology has long been associated with an increased Epstein-Barr Virus (EBV) seropositivity, viremia and cross-reactive serum antibodies specific for both virus and self. It has therefore been postulated that EBV triggers SLE immunopathology, although the mechanism remains elusive. Here, we investigate whether frequent peaks of EBV viral load in SLE patients are a consequence of dysfunctional anti-EBV CD8+ T cell responses. Both inactive and active SLE patients (n = 76 and 42, respectively), have significantly elevated EBV viral loads (P = 0.003 and 0.002, respectively) compared to age- and sex-matched healthy controls (n = 29). Interestingly, less EBV-specific CD8+ T cells are able to secrete multiple cytokines (IFN-γ, TNF-α, IL-2 and MIP-1β) in inactive and active SLE patients compared to controls (P = 0.0003 and 0.0084, respectively). Moreover, EBV-specific CD8+ T cells are also less cytotoxic in SLE patients than in controls (CD107a expression: P = 0.0009, Granzyme B release: P = 0.0001). Importantly, cytomegalovirus (CMV)-specific responses were not found significantly altered in SLE patients. Furthermore, we demonstrate that EBV-specific CD8+ T cell impairment is a consequence of their Programmed Death 1 (PD-1) receptor up-regulation, as blocking this pathway reverses the dysfunctional phenotype. Finally, prospective monitoring of lupus patients revealed that disease flares precede EBV reactivation. In conclusion, EBV-specific CD8+ T cell responses in SLE patients are functionally impaired, but EBV reactivation appears to be an aggravating consequence rather than a cause of SLE immunopathology. We therefore propose that autoimmune B cell activation during flares drives frequent EBV reactivation, which contributes in a vicious circle to the perpetuation of immune activation in SLE patients.
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