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CD11c+CD88+CD317+ myeloid cells are critical mediators of persistent CNS autoimmunity
Natalizumab, a humanized monoclonal antibody (mAb) against alpha4-integrin, reduces the number of dendritic cells (DC) in cerebral perivascular spaces in multiple sclerosis (MS). Selective deletion of α4-integrin in CD11c+ cells should curtail their migration to the CNS and ameliorate experimental autoimmune encephalomyelitis (EAE). Methods: We generated CD11c.Cre+/-ITGA4fl/fl C57/Bl6 mice to selectively delete α4-integrin in CD11c+ cells. Active immunization and adoptive transfer EAE modelsdoi:10.1101/2020.06.10.144956 fatcat:cxdsu24wa5c6djtq4vpmi5nnua