Abstract
Background. Demyelinating diseases of the central nervous system (CNS) are a heterogeneous group of disorders characterized by a damage to the myelin sheath of nerve cell axons. Multiple sclerosis (MS) is the most common chronic inflammatory demyelinating disease of the CNS affecting more than 2.9 million people worldwide. The purpose was to summarize current information about the features of the immunopathogenesis of multiple sclerosis according to the data from open sources of information. Materials and methods. The selection of publications covering the features of the immunopathogenesis of multiple sclerosis was carried out in the PubMed, Clinical Key Elsevier, Cochrane Library, eBook Business Collection and Google Scholar databases using the following keywords: multiple sclerosis, demyelinating diseases, neurodegeneration, oligodendrocytes. Results. The course of MS has three successive phases/forms known as relapsing-remitting, primary progressive and secondary progressive. Abnormalities of immune mechanisms are proposed as protagonists of the pathogenesis of MS. Autoreactive myelin-specific lymphocytes are activated outside the CNS, they cross the blood-brain barrier and form new inflammatory demyelinating lesions. The myelinating oligodendrocyte is a target during the adaptive immune response in MS. The inflammatory reaction in the brain of patients with progressive MS is observed mainly in the large connective tissues of the meninges and the periventricular space. Treatment of MS can be divided into three categories: treatment of acute relapse, disease-modifying treatment, and symptomatic treatment. Conclusions. On the T cell side, both hel-per (CD4+) and cytotoxic (CD8+) T cells are involved in the CNS damage in MS. Peripherally activated subsets of T cells (CD4+ Th1 and Th17, CD8+) migrate through the blood-brain barrier and activate B-cells and macrophages, which causes a neuroinflammatory reaction and leads to demyelination and neurodegeneration in the CNS. Oligodendrocyte progenitor cells, which are widely distributed throughout the CNS, mediate myelination and remyelination. One of the desired features of new methods for treating MS is the restoration of antigen-specific tolerance.
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