Esclerose múltipla: uma abordagem imunológica

Abstract

Objective: To address the main immunological mechanisms involved in the pathogenesis of Multiple Sclerosis, emphasizing neuroinflammation and current therapeutic interventions. Methodology: This is a narrative bibliographic review, using the databases: Capes Periodicals, Virtual Health Library and Pubmed. 55 articles published in the period from 2004 to 2019 were included. Results: The etiopathogenesis of Multiple Sclerosis involves genetic, immunological and environmental factors, which together induce processes of breaking down immune self-tolerance, neuronal injury, neuroinflammation and neurodegeneration. Neuroinflammation can be initiated by specific or foreign antigens that are exposed to leukocytes in the central nervous system. Peripheral leukocytes, especially monocytes and T and B lymphocytes, can infiltrate the nervous system due to changes in the blood-brain barrier permeability and, together with microglia, have an important role in inducing demyelinating lesions. Neurodegeneration can generate more antigenic stimuli. There are currently 17 immunomodulatory drugs approved by the Food and Drugs Administration for the treatment of the disease, but several studies are being carried out, aiming at new therapeutic approaches. Conclusion: The etiology of Multiple Sclerosis remains unknown, although current studies suggest theories about possible triggers, extrinsic and intrinsic of autoimmunity in the disease and neuroinflammation itself, the latter being an important factor inducing tissue injury and perpetuating the disease. The identification of target antigens recognized by resident T and B lymphocytes and by microglia, together with the characterization of soluble inflammatory mediators is essential to elucidate the disease's etiopathogeny and suggest new therapeutic proposals.