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Myelin autoantigens are a group of structural proteins and lipids that form the myelin sheath, a specialized membrane essential for the rapid transmission of nerve impulses and the metabolic support of axons in the central nervous system (CNS). The primary components targeted in autoimmune pathology include Myelin Basic Protein (MBP), Proteolipid Protein (PLP), and Myelin Oligodendrocyte Glycoprotein (MOG) [5, 6, 9]. In healthy individuals, these antigens are protected by the blood-brain barrier and maintained under immune tolerance; however, in demyelinating diseases like Multiple Sclerosis (MS), autoreactive T-cells and B-cells recognize these proteins as foreign, leading to chronic inflammation and neurodegeneration [7, 10]. Therapeutic strategies targeting these autoantigens focus on antigen-specific immunotherapy, which aims to reprogram the immune system to tolerate myelin without inducing broad immunosuppression. This is typically achieved by delivering myelin-derived peptides or modified antigens via nanoparticles or liver-targeting platforms to induce regulatory T-cells (Tregs) and halt the autoimmune attack [2, 3, 11]. Glatiramer acetate, a long-standing MS therapy, acts as a decoy and competitor for these antigens at the MHC interface [1].
Induction of antigen-specific immune tolerance through the expansion of regulatory T-cells (Tregs), induction of T-cell anergy or exhaustion, and competitive inhibition of Major Histocompatibility Complex (MHC) class II binding to prevent pathogenic T-cell activation [1, 11].
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