Recent advances in understanding the pathogenesis and biological treatment of multiple sclerosis.

Multiple sclerosis is the most common demyelinating disease that develops in genetically predisposed individuals through various immunopathological mechanisms induced by environmental factors, especially viral infections. Th1, Th17, γδ T cells, activated macrophages, MAIT cells, and proinflammatory cytokines, particularly IFN-γ, TNF, IL-17, and GM-CSF, are the principal pathological players whose activities cause damage to the white matter. Furthermore, a recently identified subset of CD4+ T cells has been found to migrate directly to the brain cortex and cause damage to neurons. In 2022, a new mechanism was discovered in addition to these processes. It was shown that molecular mimicry between the EBNA-1 antigen of the Epstein-Barr virus and the GlialCAM molecule of glial cells forms the basis that triggers the entire pathological process. EBV is a highly B cell-tropic human herpesvirus that placed B cells at the centre of our attention. As a result, we must down-regulate their numbers using anti-CD20 monoclonal antibodies to treat such patients (Tab. 1, Fig. 1, Ref. 37). Keywords: multiple sclerosis, GlialCAM, HLA-DR15, T-, B-, MAIT-cells, EBV, monoclonal antibodies.