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. 2020 Oct 6;11:548631. doi: 10.3389/fimmu.2020.548631

Figure 2.

Figure 2

Platelet mediated inflammation in multiple sclerosis (MS) and corresponding mice model of experimental autoimmune encephalomyelitis (EAE): Autoimmune T cells induce the breakdown of the blood-brain barrier (BBB) in multiple sclerosis. Consequently, inflammatory cells such as lymphocytes, macrophages (MΦ) and neutrophils (Ne) penetrate the BBB, promoting reactive activation of astrocytes and microglial cells and finally leading to myelin sheath destruction and axonal damage. Platelets can mediate neuroinflammation in MS/EAE by adhering to the endothelium and interacting with inflammatory and endothelial cells in various ways as depicted here. Furthermore, platelets release serotonin (5-HT), interleukin (IL)-1β and platelet activating factor (PAF), which in turn have been associated with disease progress in MS. AP, activated platelet; GP, glycoprotein; ICAM-1, intercellular adhesion molecule 1; Mac-1, macrophage-1 antigen; PSGL-1, P-selectin glycoprotein ligand-1; ROS, reactive oxygen species; VCAM-1, vascular cell adhesion protein 1; vWF, von Willebrand factor.