Myelin oligodendrocyte glycoprotein autoantibody (MOG-IgG)

Myelin oligodendrocyte glycoprotein (MOG) autoantibodies are pathogenic immunoglobulins, primarily of the IgG1 isotype, that target the MOG protein located on the surface of myelin sheaths and oligodendrocytes in the central nervous system. These antibodies are the defining biomarker and primary pathogenic driver of MOG antibody-associated disease (MOGAD), a neuroinflammatory condition distinct from multiple sclerosis and AQP4-positive neuromyelitis optica spectrum disorder (Jarius et al., 2018). Upon binding to the extracellular domain of MOG, these autoantibodies initiate complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity, leading to demyelination and axonal damage (Reindl & Waters, 2019). Clinical presentations often include optic neuritis, transverse myelitis, and acute disseminated encephalomyelitis, frequently following a relapsing course. Current therapeutic strategies focus on reducing the concentration of these autoantibodies through B-cell depletion (e.g., rituximab), enhancing IgG degradation via FcRn inhibition (e.g., efgartigimod), or physical removal through plasmapheresis. Monitoring serum MOG-IgG titers using high-sensitivity cell-based assays is critical for diagnosis, prognosis, and evaluating treatment efficacy in affected patients.

Other names

Anti-MOG antibodyMOG-AbMyelin oligodendrocyte glycoprotein antibodyAnti-MOG autoantibody

Therapeutic strategies focus on reducing the concentration of pathogenic autoantibodies through B-cell depletion to halt production, inhibition of the neonatal Fc receptor (FcRn) to accelerate IgG degradation, or physical removal via plasmapheresis (Jarius et al., 2018; Reindl & Waters, 2019).