Haghayegh Jahromi, NedaNedaHaghayegh JahromiMarchetti, LucaLucaMarchettiMoalli, FedericaFedericaMoalliDuc, DonovanDonovanDucBasso, CamillaCamillaBassoTardent, HeidiHeidiTardentBouillet, Elisa CatherineElisa CatherineBouilletDeutsch, UrbanUrbanDeutschPot, CarolineCarolinePotSallusto, FedericaFedericaSallustoStein, Jens VolkerJens VolkerSteinEngelhardt, BrittaBrittaEngelhardt0000-0003-3059-98462024-10-052024-10-052020-01-14https://boris-portal.unibe.ch/handle/20.500.12422/55985In experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS), myelin-specific T cells are activated in the periphery and differentiate in T helper (Th) 1 and Th17 effector cells, which cross the blood-brain barrier (BBB) to reach the central nervous system (CNS), where they induce neuroinflammation. Here, we explored the role of intercellular adhesion molecule-1 (ICAM-1) and ICAM-2 in the activation of naïve myelin-specific T cells and in the subsequent migration of differentiated encephalitogenic Th1 and Th17 cells across the BBB in vitro and in vivo. While on antigen-presenting cells ICAM-1, but not ICAM-2 was required for the activation of naïve CD4+ T cells, endothelial ICAM-1 and ICAM-2 mediated both Th1 and Th17 cell migration across the BBB. ICAM-1/-2-deficient mice developed ameliorated typical and atypical EAE transferred by encephalitogenic Th1 and Th17 cells, respectively. Our study underscores important yet cell-specific contributions for ICAM-1 and ICAM-2 in EAE pathogenesis.enICAM-1 ICAM-2 T cell activation Th1 cells Th17 cells blood-brain barrier dendritic cells experimental autoimmune encephalomyelitis600 - Technology::610 - Medicine & healtharticle10.48350/1508493199305910.3389/fimmu.2019.03056