Myelin oligodendrocyte glycoprotein-reactive B cell receptor (MOG-BCR)

Myelin oligodendrocyte glycoprotein (MOG)-reactive B cell receptors (BCRs) and their corresponding autoantibodies are central pathological components in central nervous system (CNS) demyelinating disorders, most notably MOG antibody disease (MOGAD). These receptors specifically target the extracellular IgV domain of full-length MOG, which is expressed on the surface of myelin sheaths and oligodendrocytes (Jarius et al., 2018). Upon binding, these antibodies facilitate complement-dependent cytotoxicity and recruit inflammatory cells, leading to the destruction of myelin and subsequent axonal damage (Reindl & Waters, 2019). While MOG is the primary target, these B cells can exhibit cross-reactivity or contribute to epitope spreading, where the immune response expands to include other myelin proteins like myelin basic protein (MBP) (Pröbstel et al., 2011). In clinical practice, the detection of these antibodies using live cell-based assays is the gold standard for diagnosing MOGAD and differentiating it from multiple sclerosis. Current therapeutic approaches focus on reducing the population of MOG-specific B cells or neutralizing the circulating antibodies to prevent clinical relapses and permanent neurological disability (Weber et al., 2018).

Other names

Anti-MOG antibodyMOG-specific B cell receptorMyelin-reactive B cell receptorMOG-IgGCross-reactive myelin B cell receptor

Therapeutic strategies involve the depletion of B cells expressing these receptors via anti-CD20 or anti-CD19 monoclonal antibodies, the use of FcRn inhibitors to accelerate the clearance of pathogenic IgG, and the inhibition of the complement cascade to prevent antibody-mediated myelin destruction (Reindl & Waters, 2019; Weber et al., 2018).