The Plasticity of Immune Cell Response Complicates Dissecting the Underlying Pathology of Multiple Sclerosis

Figure 1

The role of immune cells in multiple sclerosis. An autoinflammatory reaction is triggered by an aberrant immune reaction due to epigenetic and environmental risk factors in genetically predisposed individuals. There is infiltration of immune cells into the brain (peripheral autoreactive T cells activated with myelin basic protein (MBP), proteolipid protein (PP), myelin oligodendrocyte glycoprotein (MOG), cross the blood–brain barrier (BBB) and enter the central nervous system (CNS), infiltrating other T cells, and APCs to enhance neuroinflammation). In healthy brain, Treg cells suppress autoreactive T cells, but under autoimmune conditions, the autoimmune suppressive activity of Treg cell is disrupted. B cell trafficking is influenced by many chemokines, including CXCL13, and they present antigens and release antibodies. Macrophages and microglia release cytokines and chemokines damaging the myelin sheath; while there is antigen uptake by dendritic cells (DCs) and CD4 T cell/DC interactions, and the interaction of several other immune cells, resulting in demyelination of the neuron (created with https://BioRender.com).