EBI2 is expressed in glial cells in multiple sclerosis lesions, and its knock?out modulates remyelination in the cuprizone model

EBI2 receptor regulates the immune system, and in multiple, sclerosis is upregulated central nervous system infiltrating lymphocytes. In newborn EBI2-deficient mice, myelin development delayed, its persistent antagonism inhibits remyelination chemically demyelinated organotypic cerebellar slices. We used cuprizone model of multiple to elucidate role system-expressed de- remyelination. The wild-type knock-out mice were fed 0.2% chow for 5 weeks allowed recover on a normal diet 2 weeks. data showed less efficient recovery myelin, attenuated oligodendrocyte loss, fewer astrocytes increased total cholesterol levels after recovery. Moreover, expression confirming involvement signalling during from demyelination model. pro-inflammatory cytokine at comparable with only minor differences TNF? IL1? either peak or neuroinflammatory molecules, Abl1 kinase NF?B1 (p105/p50) subunit, significantly downregulated disease. Immunohistochemical investigations distribution (CNS) cells (MS) brain revealed strong microglia inside plaques implicating glia-expressed pathophysiology. Taken together, these findings demonstrate rather than as such warrant further research into