A recent study published in Science Translational Medicine has uncovered a critical role of Epstein–Barr virus (EBV) in the progression of systemic lupus erythematosus (SLE), an autoimmune disease affecting approximately five million people globally. Researchers from Stanford University utilized an EBV-specific single-cell RNA-sequencing platform to demonstrate that EBV reprograms autoreactive B cells into antigen-presenting cells, thereby exacerbating autoimmunity in SLE patients.
William Robinson, MD, PhD, the study’s corresponding author, emphasized the significance of this finding, suggesting it may apply to all lupus cases. The research highlights the complexities involved in understanding EBV’s mechanisms, particularly given its lifecycle and the low prevalence of infected B cells in healthy individuals. In SLE patients, however, this prevalence increases dramatically, suggesting a direct link between EBV infection and the disease’s severity.
Moreover, the study indicates that EBV triggers the transcription factor EBNA2, which activates pro-inflammatory genes, thereby recruiting helper T cells that stimulate the immune response. Robinson posits that this EBV-driven mechanism may extend beyond SLE, potentially implicating other autoimmune diseases such as multiple sclerosis and rheumatoid arthritis. As the majority of the population carries latent EBV, the study raises critical questions about the specific triggers that lead to autoimmunity in a subset of individuals, underscoring the need for further research in this area.
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