fig1

Figure 1. Pathogenesis of multiple sclerosis and targets of drug action. ➀ Reduced production of Th1 and Th17 cells and Th1-Th2 shift (interferon-β, teriflunomide, dimethyl fumarate); ➁ Competitive binding of MHC class II molecules (glatiramer acetate); ➂ Depletion of CD20-positive lymphocytes (ocrelizumab, rituximab); ➃ Regulation of T-cells, B-cells, NK cells, and dendritic cells (interferon-b, glatiramer acetate); ➄ Depletion of CD52-positive lymphocytes (alemtuzumab); ➅ Alteration of lymphocyte distribution (fingolimod); ➆ Preventing activated CD4+ T-cells from crossing the blood-brain barrier (natalizumab, interferon-β); ➇ Promoting leukocyte migration to the central nervous system (glatiramer acetate). VLA-4: very late antigen-4; MMP: matrix metalloproteinase; MHC: major histocompatibility complex; IFN: interferon; IL: interleukin; NK: natural killer; TCR: T-cell receptor; Th: T helper