RNA Editing Profiles and Distinct Immune Responses in Myelin Oligodendrocyte Glycoprotein Antibody-Positive Optic Neuritis

To characterize adenosine-to-inosine (A-to-I) RNA editing in myelin oligodendrocyte glycoprotein antibody-positive optic neuritis (MOG-ON), explore phase-based immune response differences, and screen therapeutic targets and visual prognosis factors, we collected 14 peripheral blood samples from patients with MOG-ON (9 acute, 5 remission) and 7 healthy volunteers, screened differentially edited sites and genes, conducted functional enrichment, compared stage-wise gene and immune pathway profiles, and quantified immune cell subsets via CIBERSORTx; MOG-ON patients exhibited widespread editome remodeling with 240 differential edited sites and 135 genes enriched in neutrophil immunity and T-cell differentiation, with ITGAX and C5AR1 as core regulators; acute-phase pathways centered on immunoglobulin and B cell receptor signaling, while cell cycle pathways prevailed in remission; Toll-like receptor and MAPK pathways mediate inflammatory myelin damage, and cytochrome P450, pyrimidine and collagen metabolism support anti-inflammatory neural repair; UBB and CD74 were acute hub genes, CDK1 the remission hub gene; CD74 correlated positively with neutrophils and negatively with monocytes, and CDK1 correlated positively with M0 macrophages and memory B cells; acute BCVA correlated with regulatory T cells and memory B cells, while remission BCVA correlated with monocytes and resting CD4+ memory T cells; our findings confirm abnormal A-to-I editing modulates immune-inflammatory networks to drive MOG-ON pathogenesis and identify stage-specific immune signatures, providing new evidence for precise diagnosis and targeted therapy of MOG-associated optic neuritis.