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Figure 1: T-cell model of MS immunopathogenesis. Damage to the CNS occurs in sequential steps. Th1 cells are activated in the periphery by antigen-presenting cells (APCs) such as DCs (step 1). After activation, these cells adhere to the endothelial cell layer lining the blood-brain-barrier “BBB” (step 2). Activated cells are attracted towards chemotactic molecules, including the chemokines (step 3). The cells invade the CNS tissues (step 4). These invaders are reactivated in the CNS by either resident APCs like microglia cells, or by migrating DCs (step 5). The figure also explains the interaction of inflammatory T cells (Th1 or Th17) and GA-reactive T cells in the CNS. In this model, the autoreactive Th1 or Th17 cells as well as GA-reactive T cells arrive into the CNS. In the CNS, GA-reactive T cells secrete the beneficiary molecules IL-4, IL-5, IL-10, and BDNF which counteract the effects of the inflammatory molecules IL-2, IL-17, or IFN-γ released by Th1 or Th17 cells. The latter cells may also downregulate the expression of chemokine receptors on the surface of GA-reactive T cells, making them unable to migrate into the desired areas in the brain [16].