Advances in the immunopathogenesis of multiple sclerosis

Abstract

A better understanding of immune-mediated mechanisms in the pathogenesis of multiple sclerosis and the contribution of environmental risk factors toward the development of multiple sclerosis will help further improve therapeutic approaches to prevent disease progression.

IL-27-induced modulation of autoimmunity and its therapeutic potential

“…MS is an autoimmune disease that affects the brain and the spinal cord, and it is characterized by neuroinflammation as well as neurodegeneration caused by the depletion of myelin in the central nervous system (CNS) [80, 81]. The pathogenesis of MS involves Th1 and Th17 responses to myelin antigens [80, 81].…”

“…The pathogenesis of MS involves Th1 and Th17 responses to myelin antigens [80, 81]. The level of IL-27 in the plasma/serum from MS patients was found to be significantly lower than that of healthy controls [82-84], and IL-27 level showed an inverse correlation with the level of plasma IL-17 as well as the frequency of Th17 cells in the blood [82].…”

Melanocortin-1 receptor activation is neuroprotective in mouse models of neuroinflammatory disease

“…They are known to be mediated by peripherally generated autoreactive T-cells infiltrating into the CNS, where they are re-stimulated by antigen-presenting cells, resulting in local expansion of pathogenic Th1 and Th17 cells, tissue damage to oligodendrocytes, and subsequently, a secondary infiltration of bystander immune cells, controlling the disease's perpetuation (2,3). Regulatory T-cells (Treg) are involved in limiting the activation, proliferation and infiltration of pathogenic effector cells into the CNS (1, 4).…”

Toll-like receptor-mediated immune responses in intestinal macrophages; implications for mucosal immunity and autoimmune diseases

“…Multiple sclerosis (MS) is an autoimmune disease of the central nervous system (CNS) that is characterized by peripheral inflammatory processes, blood-brain barrier (BBB) breakdown, and immune cell infiltration into the CNS, leading to both axonal damage and demyelination, and ultimately resulting in disability in MS patients [152–154]. Previous studies showed that high salt not only potentiates LPS-induced macrophage activation, including enhanced IL-1α, TNF-α and IL-1β production, but also enhances the development of MS partly through changing the gut microbiome [153, 155–160].…”