• Bratisl Med J · Jan 2023

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

    • Milan Buc.
    • Bratisl Med J. 2023 Jan 1; 124 (12): 903906903-906.

    AbstractMultiple 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.

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