Multiple sclerosis (MS) is a chronic autoimmune demyelinating disease of the central nervous system in which autoreactive T cells (CD4+ Th1 and Th17 cells) cross the blood-brain barrier and orchestrate an inflammatory attack against myelin sheaths and oligodendrocytes. This inflammatory cascade involves activation of microglia, recruitment of B cells producing anti-myelin antibodies, complement activation, and release of cytokines (TNF-alpha, interferon-gamma, IL-17) that directly damage myelin and axons. Demyelination disrupts saltatory conduction along affected nerve fibers, producing the clinical manifestations of relapse (optic neuritis, myelitis, brainstem syndromes). Repeated inflammatory episodes lead to progressive axonal degeneration, gliotic scar formation (the sclerotic plaques for which the disease is named), and irreversible neurological disability. Disease-modifying therapies (DMTs) target specific immunological mechanisms: injectable platform therapies (interferon beta reduces T-cell activation and pro-inflammatory cytokine production; glatiramer acetate acts as a decoy myelin basic protein, shifting immune response from Th1 to Th2); oral agents (fingolimod sequesters lymphocytes in lymph nodes by downregulating sphingosine-1-phosphate receptor 1; dimethyl fumarate activates the Nrf2 antioxidant pathway and induces lymphocyte apoptosis; teriflunomide inhibits dihydroorotate dehydrogenase, blocking pyrimidine synthesis in rapidly dividing lymphocytes);...