biostudies-literatureKozela EDr. Miriam and Sheldon G. Adelson Medical Research FoundationNINDS NIH HHSNINDS Informatics Center for Neurogenetics and Neurogenomics136https://www.ebi.ac.uk/biostudies/studies/S-EPMC4891926biostudies-literatureUnknown13(1)<h4>Background</h4>Our previous studies showed that the non-psychoactive cannabinoid, cannabidiol (CBD), ameliorates the clinical symptoms in mouse myelin oligodendrocyte glycoprotein (MOG)35-55-induced experimental autoimmune encephalomyelitis model of multiple sclerosis (MS) as well as decreases the memory MOG35-55-specific T cell (TMOG) proliferation and cytokine secretion including IL-17, a key autoimmune factor. The mechanisms of these activities are currently poorly understood.<h4>Methods</h4>Herein, using microarray-based gene expression profiling, we describe gene networks and intracellular pathways involved in CBD-induced suppression of these activated memory TMOG cells. Encephalitogenic TMOG cells were stimulated with MOG35-55 in the presence of spleen-derived antigen presenting Journal of neuroinflammationPathways and gene networks mediating the regulatory effects of cannabidiol, a nonpsychoactive cannabinoid, in autoimmune T cells.PMC4891926P30 NS062691Juknat AVogel ZKozela EKaushansky NGao FCoppola GfalsePathways and gene networks mediating the regulatory effects of cannabidiol, a nonpsychoactive cannabinoid, in autoimmune T cells.<h4>Background</h4>Our previous studies showed that the non-psychoactive cannabinoid, cannabidiol (CBD), ameliorates the clinical symptoms in mouse myelin oligodendrocyte glycoprotein (MOG)35-55-induced experimental autoimmune encephalomyelitis model of multiple sclerosis (MS) as well as decreases the memory MOG35-55-specific T cell (TMOG) proliferation and cytokine secretion including IL-17, a key autoimmune factor. The mechanisms of these activities are currently poorly understood.<h4>Methods</h4>Herein, using microarray-based gene expression profiling, we describe gene networks and intracellular pathways involved in CBD-induced suppression of these activated memory TMOG cells. Encephalitogenic TMOG cells were stimulated with MOG35-55 in the presence of spleen-derived antigen presenting 2016-01-01T00:00:00Z2016 Jun2026-06-14T09:51:41.965Z2019-03-27T02:15:15ZS-EPMC48919262725634310.1186/s12974-016-0603-x