Досрочная реакция в цитокине и miR-124, -125b, -223 на антиCD20 в Множестве склероза и его животной модели - предварительный анализ.
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Orefice Nicola Salvatore, Amoriello Roberta, Maghrebi Olfa, Ballerini Chiara, Baldi Giovanni, Arpino Roberta, Abate Marianna, Zappavigna Silvia, Pastò Luisa, Amato Maria Pia, Caraglia Michele, Ballerini Clara
Аннотация
Оригинал публикации
Early response in cytokine and miR-124a, -125b, -223 expression to anti-CD20 in Multiple Sclerosis and its animal model - a preliminary analysis.
INTRODUCTION: Multiple Sclerosis (MS) is an autoimmune, demyelinating, inflammatory disorder. The anti-CD20 monoclonal antibody ocrelizumab targets B cells, effectively controlling the disease. MicroRNAs (miRNAs), small molecules modulating immune responses and neuroinflammation, may serve as biomarkers for disease progression, though the impact of anti-CD20 remains unclear. We hereby selected three miRNAs of interest for their relevance in experimental autoimmune encephalomyelitis (EAE) and MS, miR-124a-3p, miR-125b-5p, and miR-223-3p.
METHODS: We examined these miRNAs in the spinal cord of EAE mice treated with a nanoformulation of anti-CD20 and in 23 MS patients' serum (19 relapsing-remitting [RR] and 4 primary-progressive [PP]) before (T0) and after six months (T6) of ocrelizumab, alongside with serum cytokines and chemokines.
RESULTS: We found reduced (*p = 0.045) miR-223-3p in nano-anti-CD20-treated mice and in patients (*p = 0.030) with inactive MS. RRMS showed varying miRNA expression, while PPMS exhibited reduced (*p = 0.029) miR-124a-3p at T6. CXCL10 was elevated (*p = 0.024) in patients with active MS. Overall, six cytokines increased at T6, with interleukin 6 (IL6) negatively correlating with miR-223-3p. Gene analysis showed that IL6 gene is among miRNAs' targets, alongside inflammatory pathways.
CONCLUSIONS: This is the first study to compare miR-124a-3p, miR-125b-5p, and miR-223-3p in both EAE and MS patients undergoing anti-CD20 therapy, suggesting subtype-specific molecular responses, identifying miR-223-3p as a potential biomarker of treatment response, and highlighting immune regulatory pathways as key mechanisms linking these miRNAs to disease progression and therapy outcomes.