<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE339nnn/GSE339140/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Homo sapiens</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE339140</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>RNA Editing Profiles and Distinct Immune Responses in Myelin Oligodendrocyte Glycoprotein Antibody-Positive Optic Neuritis</name><description>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.</description><dates><publication>2026/09/23</publication></dates><accession>GSE339140</accession><cross_references><GSM>GSM9889033</GSM><GSM>GSM9889022</GSM><GSM>GSM9889032</GSM><GSM>GSM9889021</GSM><GSM>GSM9889031</GSM><GSM>GSM9889020</GSM><GSM>GSM9889030</GSM><GSM>GSM9889026</GSM><GSM>GSM9889015</GSM><GSM>GSM9889014</GSM><GSM>GSM9889025</GSM><GSM>GSM9889013</GSM><GSM>GSM9889024</GSM><GSM>GSM9889023</GSM><GSM>GSM9889019</GSM><GSM>GSM9889029</GSM><GSM>GSM9889018</GSM><GSM>GSM9889028</GSM><GSM>GSM9889017</GSM><GSM>GSM9889016</GSM><GSM>GSM9889027</GSM><GPL>24676</GPL><GSE>339140</GSE><taxon>Homo sapiens</taxon><PMID>[42756340]</PMID></cross_references></HashMap>