An unknown antigen presented by the major histocompatibility complex (MHC) class II molecules causes T cells to become autoreactive (Fig. 29-1). Once activated, T cells penetrate the blood-brain barrier by attachment to upregulated adhesion molecules and production of matrix metalloproteinases (MMP) that cause blood-brain barrier breakdown. In the CNS, the T cells come into contact with antigen-presenting cells (APCs) and proliferate. The T-helper cells differentiate into proinflammatory T-help-er-1 cells (Th1 cells) and anti-inflammatory T helper-2 cells (Th2 cells).8 Th1 cells secrete cytokines that enhance macrophage and microglial cells that attack myelin.8

B cells cross previously damaged sections of the blood-brain barrier to arrive in the CNS, an area normally free of B cells. Autoreactive T cells trigger B cells to form myelin autoantibodies. B-cell antibodies also initiate the complement cascade, causing myelin degradation.8 These inflammatory processes probably cause relapses.5

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