OMG抗体

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     Gel: 8%SDS-PAGE, Lysate: 40 μg, Lane: Mouse brain tissue, Primary antibody: P05119(OMG Antibody) at dilution 1/200, Secondary antibody: Goat anti rabbit IgG at 1/8000 dilution, Exposure time: 20 seconds    

  
  

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     The image is immunohistochemistry of paraffin-embedded Human tonsil tissue using P05119(OMG Antibody) at dilution 1/30. (Original magnification: ×200)    

  
  

The oligodendrocyte myelin glycoprotein (OMG) antibody is associated with autoimmune responses targeting myelin in the central nervous system (CNS). OMG, a glycoprotein expressed on oligodendrocytes and myelin sheaths, plays a role in axon guidance and myelination. Initially identified in the 1990s, OMG became a focus in neuroimmunology due to its potential link to demyelinating disorders like multiple sclerosis (MS). Autoantibodies against OMG are thought to contribute to myelin destruction by triggering immune-mediated attacks, disrupting nerve signal transmission.

Research highlights OMG antibodies in a subset of MS patients and other CNS inflammatory conditions, though their pathogenic role remains debated. Unlike well-characterized targets like myelin basic protein (MBP) or myelin oligodendrocyte glycoprotein (MOG), OMG antibodies are less studied, partly due to overlapping epitopes with other myelin antigens. Animal models show that OMG-specific antibodies can induce demyelination, supporting their potential involvement in autoimmune mechanisms.

Recent studies explore OMG antibodies as diagnostic or prognostic biomarkers, particularly in atypical demyelinating cases. However, clinical utility is limited by variability in detection methods and inconsistent associations across patient cohorts. Current investigations also aim to clarify whether OMG antibodies are primary drivers of disease or secondary markers of myelin damage. Therapeutic strategies targeting OMG, such as B-cell depletion or antibody-neutralizing approaches, remain experimental but may hold promise for personalized treatments in neuroinflammatory disorders.