Abstract
Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system (CNS) and the pathogenesis leading to demyelination includes 3 major processes. The first step is establishment of autoimmunity to CNS myelin components, with molecular mimicry between a portion of the infectious agents and that of myelin, which is an important feature. The second step is entry of immune cells into the CNS via the blood-brain barrier (BBB). Activated T cells can easily cross the BBB using surface LFA-1 and VLA-4 as ligands to ICAM-1 and VCAM-1, respectively, which are expressed on endothelial cells in the CNS. As the third step, immune reactions occur within the CNS when activated T cells encounter specific antigens presented by microglia. Of the helper T cells re-stimulated by autoantigens, Th1 cells producing interferon-γ and Th17 cells secreting interleukin-17 play major roles in propagating inflammation, while Th2 cells producing IL-4, and regulatory T cells secreting IL-10 and TGF-β suppress pathological processes. Final demyelination is rendered either by macrophages recruited from the bloodstream across the BBB, or by TNF-α and nitric oxide, which are secreted by Th1 cells and macrophages, and toxic to CNS myelin.
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