MOG抗体—艾普蒂

+ +

•  

   

     Gel: 12%SDS-PAGE, Lysate: 40 μg, Lane 1-4: Mouse brain tissue, Rat brain tissue, Human cerebrum tissue, Human cerebella tissue lysates, Primary antibody: P05919(MOG Antibody) at dilution 1/250, Secondary antibody: Goat anti rabbit IgG at 1/8000 dilution, Exposure time: 3 seconds    

  
  

•  

   

     The image is immunohistochemistry of paraffin-embedded Human breast cancer tissue using P05919(MOG Antibody) at dilution 1/25. (Original magnification: ×200)    

  
  

Myelin oligodendrocyte glycoprotein (MOG) antibodies target MOG, a protein expressed on the surface of oligodendrocytes and myelin sheaths in the central nervous system (CNS). Initially studied in the context of experimental autoimmune encephalomyelitis (EAE), MOG was considered a potential autoantigen in multiple sclerosis (MS). However, research over the past decade has redefined MOG antibody-associated disease (MOGAD) as a distinct clinical entity, separate from MS and aquaporin-4 (AQP4) antibody-positive neuromyelitis optica spectrum disorder (NMOSD).

MOGAD predominantly presents with optic neuritis, transverse myelitis, or acute disseminated encephalomyelitis (ADEM)-like syndromes, often affecting both adults and children. Unlike AQP4 antibodies, MOG antibodies are predominantly IgG1 and appear to directly target conformational epitopes of the MOG protein. Diagnosis relies on cell-based assays (CBA) using full-length human MOG, as older ELISA methods lacked specificity.

Clinically, MOGAD often shows better recovery with steroids compared to NMOSD, though relapses occur in ~40% of cases. While initially considered monophasic, recurrent forms are increasingly recognized. Treatment typically involves immunosuppressants like corticosteroids, IVIG, or rituximab for relapsing cases. Ongoing research aims to clarify its pathophysiology, long-term outcomes, and optimal therapeutic strategies, highlighting its evolving significance in neuroinflammatory disorders.