Role of Exosomes in Multiple Sclerosis

Multiple sclerosis (MS) is a central nervous system (CNS) autoimmune disease in which autoreactive immune cells recognize myelin antigens and cause demyelination and axonal damage. Inflammatory CD4+ T cells that are responsive to myelin peptides primarily recognize myelin and oligodendrocytes as their targets. Regulatory CD4+ T (Treg) cells typically maintain immune system homeostasis by blocking the negative effects of inflammatory T cells. However, for an unknown reason, Treg cell numbers are lower in MS patients. Particularly those underlying the start of immune system dysfunction, mechanisms important to the MS pathogenesis have not yet been fully understood. For instance, the peripheral immune system’s mechanism for producing reactivity to CNS components is unknown. This commentary focuses on a unique way that exosomes in the bloodstream operate in multiple sclerosis (MS): they prevent Treg cells from differentiating. According to recent findings, exosomes are endosome-derived microvesicles that are 30–200 nm in size and carry specialized protein and RNA cargo. These cells are thought to release these exosomes. The idea that exosomes could influence signalling between brain cells and enhance the distribution of bioactive substances is raised by the fact that exosomes can interact with nearby cells. In addition to myelinating axons, oligodendrocytes also preserve axonal integrity via an unidentified trophic support mechanism. These exosomes stimulate pre-oligodendrocytes to develop into myelin-producing cells in the brain, greatly increasing myelination and improving demyelination after damage. They also have a high potential as a treatment since they are non-toxic and quickly traverse the blood–brain barrier. A novel perspective on the study of the pathophysiology of this disease should be offered by increased knowledge of exosome-dependent pathways in MS. Exosomes and their contents may function as biomarkers in MS.