ArticleAnnals of neurology2026
Proinflammatory Epstein-Barr Virus Antibody Functions Track with Disease Activity in Multiple Sclerosis.
Article in Annals of neurology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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10 authors.
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Abstract
objectiveEpstein-Barr virus (EBV) has been implicated in the pathogenesis of multiple sclerosis (MS). Elevated immunoglobulin G (IgG) titers against EBV nuclear antigen 1 (EBNA1) represent the most consistent serological marker of MS risk, with levels remaining persistently elevated following disease onset.
methodsWe conducted high-dimensional profiling of virus-specific antibody-associated immune features in 60 individuals with relapsing-onset MS followed over time and in 54 age- and sex-matched EBV-seropositive healthy controls.
resultsEBNA1-specific IgG in MS patients exhibited a distinct proinflammatory Fc signature, characterized by increased affinity for Fc γ receptors (FcγRs) and enhanced Fc-mediated effector functions, including antibody-dependent phagocytosis, complement activation, and natural killer cell engagement. This signature was not observed for antibodies against other common viral antigens and showed a strong association with MS. Increased FcγR binding by IgG, specific for both EBNA1 and the lytic EBV glycoprotein 350 (EBV-gp350) correlated with disease activity, defined as clinical relapse and/or presence of contrast-enhancing brain lesions (CELs).
interpretationBoth fragment antigen-binding and pro-inflammatory functional Fc-mediated features contribute to the association between EBNA1-specific antibody responses and MS. Fc effector functions of EBV-specific antibodies may actively participate in promoting focal disease activity in MS. ANN NEUROL 2026;100:547-558.
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