Fig. 3
From: The brain cytokine orchestra in multiple sclerosis: from neuroinflammation to synaptopathology
EAE pathogenesis. EAE can be induced in mice by active immunization with encephalitogenic peptide antigen such as the myelin oligodendrocyte glycoprotein 35–55 (MOG35–55). Peripheral dendritic cells (DCs) present the antigen to naïve T lymphocytes that are primed to differentiate into T helper 1 (Th1) and Th17 phenotypes, upon interleukin-12 (IL-12) and IL-23, respectively. Monocytes are also recruited and stimulated to differentiate into macrophages upon macrophage inflammatory protein-1 (MIP-1). Activated cells express adhesion molecules and pass through the blood–brain barrier (BBB) endothelium entering the central nervous system (CNS). Local CNS-antigen presenting cells (APCs) reinforce myelin-specific Th1 and Th17 effector and macrophages response. Activated cells produce pro-inflammatory cytokines (CKs) and chemokines that fuel myelin damage [69, 70]. Parts of the figure were drawn by using pictures from Servier Medical Art. Servier Medical Art by Servier is licensed under a Creative Commons Attribution 3.0 Unported License (https://creativecommons.org/licenses/by/3.0/)