We need to talk about MOG

Autoantibody assays detect the presence of antibodies to specific self-targets. These antibodies can be disease associated, causative, or part of the normal repertoire. Our understanding of where myelin oligodendrocyte glycoprotein (MOG) immunoglobulin G (IgG) sits in this context is still evolving. MOG antibodies, when tested by cell-based assay at a dilution of 1:20, are found in the sera of healthy people and in any disease cohort screened.¹ A serum dilution of 1:160 was selected to identify people with high-titer MOG antibodies who have a more limited clinical picture, which is still not uniform. For example, the presenting features can be age dependent, with acute disseminating encephalomyelitis (ADEM) the predominant presentation in young children while optic neuritis is more common in children >11 years of age and adults.^2,3 In addition, patients with MOG antibodies have a different disease course and outcomes that may not be modified by the presence of the antibody. Recent work suggests that 50% of cases of pediatric ADEM will be positive for MOG antibodies, but the presence of MOG antibodies, in the absence of additional clinical features, does not appear to modify the relapse risk. In contrast, most children who present with ADEM in association with optic neuritis or transverse myelitis are MOG antibody positive, and these children have a largely relapsing disease course.³ Hence, even though we have improved the MOG-IgG test specificity, MOG antibodies are still associated with a range of clinical courses and outcomes, which complicates treatment evaluation and clinical trials.