Introduction: Multiple sclerosis is a chronic inflammatory disorder characterized by the demyelination of central nervous system neurons, giving rise to various motor and non-motor impairments. Aging has been strongly associated with inflammation and immunosenescence, and it is believed that the dysfunction of regulatory T-cells is the central complication in the maintenance of peripheral immunity. CD4+ T-cells and Th17 cells seem to play a crucial role in autoimmune inflammation and are important in the pathophysiology underlying multiple sclerosis. In this systematic review, the link between aging and T-cell function will be explored as well as its implication in MS pathophysiology.
Methods: A literature review was conducted using databases such as PubMed, NCBI, and Scopus. Relevant primary literature describing theories or results of an experiment and review papers were selected. Data from primary articles were analyzed to explore the association between aging and MS, as well as its contribution to immunosenescence.
Results: There exists a strong association between aging and the pathophysiology of MS which was suggested by a multitude of laboratory studies. Animal models of experimental autoimmune encephalomyelitis have demonstrated the immunological mechanisms of this disease by highlighting differences in T-cell presence and function in healthy people versus MS patients.
Discussion: According to numerous studies, chronic inflammation is recognized as a sign of aging, rendering it one of the key contributors to neurodegenerative diseases like MS. The implication of regulatory T-cells in MS is crucial due to its necessity for the maintenance of immunosuppressive activity, which has been found to deteriorate with age. Myelin antigens supplied by microglial cells reactivate autoreactive CD4+ T-cells infiltrating the CNS, producing a cascade of immunological responses that lead to demyelination and tissue death.
Conclusion: This literature review finds that MS is largely T-cell mediated and that the aging process heightens chronic inflammation, leading to the destruction of neurons in the CNS.
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