The EBV-autoimmunity axis: mechanistic insights in SLE, MS and PSC

EBNA2-Mediated Host Enhancer Hijacking and B cell Reprogramming described by Younis et al.² (a) Latent EBNA2 replicates within EBV-infected CD27⁺ CD21^low memory B cells. (b) Acting as a powerful epigenetic remodeler, EBNA2 binds to the host cell enhancer regions and disrupts the natural B-cell identity to "hijack" the host genome. (c) This increases the antigen-presenting cell (APC) transcriptomic function, leading to a profound immunophenotypic shift marked by the upregulation of TBX21 (T-bet), ZEB2 and the machinery required for MHC class II antigen presentation. This reprogramming turns a dormant memory B cell into a hyper-efficient APC.