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Abstract

Multiple sclerosis (MS) is a chronic, inflammatory, and neurodegenerative disorder of the central nervous system (CNS) characterized by immune-mediated damage to myelin, oligodendrocytes, and axons. T-cells, particularly CD4+ T-helper cells and CD8+ cytotoxic T-cells, are central to the pathogenesis of MS. These immune cells mediate neuroinflammation, leading to demyelination and neuronal damage. In recent years, our understanding of the specific T-cell subtypes involved in MS has significantly evolved, highlighting the roles of Th1, Th17, and regulatory T-cells (Tregs) in both the onset and progression of the disease. This review explores the mechanisms by which T-cells mediate neuroinflammation in MS, emphasizing the cellular pathways involved and their impact on disease progression. The review also addresses potential therapeutic strategies aimed at modulating T-cell responses, with a focus on immunotherapies that may help prevent or slow the disease's debilitating course. Further research into the molecular and cellular interactions underlying T-cell-mediated neuroinflammation is critical for the development of more effective and personalized treatments for MS patients.