ArticleJournal of neurology2026
Antiviral and inflammatory immune signatures in anti-CD20-treated multiple sclerosis: a cross-sectional study.
Article in Journal 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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19 authors.
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Abstract
CD20-targeting monoclonal antibodies are highly effective therapies for relapsing multiple sclerosis (MS). We examined how anti-CD20 therapy reshapes antiviral T-cell immunity, innate inflammatory tone, and blood markers of neuroaxonal injury. In this cross-sectional study, adults with relapsing MS were enrolled at two neurological centers in Rome. An immunophenotyping cohort (45 untreated, 25 anti-CD20-treated, all receiving ocrelizumab) was profiled by high-parameter flow cytometry across more than 40 immune populations. A separate antiviral cohort (24 untreated, 13 treated, 19 healthy donors) was assessed for T-cell responses to Epstein-Barr virus (EBV), cytomegalovirus (CMV) and SARS-CoV-2 by activation-induced marker assay, for cytokine and chemokine release by multiplex assay, and for serum neurofilament light chain (sNfL) by single-molecule array. Groups were compared by Kruskal-Wallis with Dunn's correction; correlations used Spearman's rank test. Anti-CD20 therapy depleted total and switched-memory B cells while sparing antibody-secreting cells and reduced absolute counts of follicular helper T cells and mucosal-associated invariant T cells. Untreated patients with MS (pwMS) showed elevated monocyte interleukin-1β and monocyte chemotactic protein-3 (MCP-3) and impaired pDC cell interferon-α production, whereas pDC IFN-α responses in ocrelizumab-treated pwMS were comparable to those in HD. EBV-specific CD4+ T-cell counts and stimulation index were selectively lower ocrelizumab-treated pwMS, whereas CMV- and SARS-CoV-2-specific responses were comparable across groups. sNfL was elevated in untreated pwMS and correlated with MCP-3 at baseline and after EBV stimulation. Anti-CD20 therapy acts on immune circuits beyond B cells, selectively contracting EBV-directed helper T-cell immunity while sparing other antiviral responses, and identifies MCP-3 as a candidate blood marker associated with neuroaxonal injury in pwMS.
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