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Fig. 1 | Journal of Neuroinflammation

Fig. 1

From: Aberrant DNA methylation profile exacerbates inflammation and neurodegeneration in multiple sclerosis patients

Fig. 1

The underlying pathophysiological mechanism of MS. In the first instance, autoreactive CD4+ T cells are activated in the periphery by antigen presenting cells (APC) that present, in conjunction with class II MHC molecules, similar antigens to those synthesised by the CNS. (1) This interaction activates the differentiation of CD4+ T naïve cells into CD4+ T helper cells (Th). (2) Upon activation, Th produces interferon-gamma (IFN-γ), a cytokine responsible for recruiting CD8+ T cells, B cells and monocytes in the periphery. (3) These proinflammatory cells migrate to the blood–brain barrier (BBB) and pass into the CNS. Inside the brain, plasma B cells produce auto-antibodies against CNS self-antigens contributing to myelin sheath damage. This process is aggravated when infiltrated cytotoxic CD8+ T cells attack oligodendrocytes causing their destruction and neuronal death. Monocytes, on the other hand, increase local inflammatory response by releasing proinflammatory cytokines and contributing to demyelination through myelin phagocytosis. (4) In parallel, infiltrated CD4+ T cells are reactivated upon interaction with myelin fragments presented by resident APCs which favours (5) proinflammatory cytokines and chemokines release, (6) astrogliosis and microgliosis

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