Table 7 The present study investigates the impact disease-modifying therapy (DMT) medications on several immune cell populations, with a particular focus on the underlying processes including mitochondrial and metabolic dysfunction
From: Mitochondrial and metabolic dysfunction of peripheral immune cells in multiple sclerosis
DMT drugs | Immune cell type | Mechanism of mitochondrial and metabolic dysfunction | References |
|---|---|---|---|
Interferon beta | T cell | Reverse the decreased glycolysis and mitochondrial respiration activity by upregulating the expression of aldolase, HK-1, ENO1, GLUT1, DLAT and DLST | [77] |
DC | Suppress the differentiation of Th17 cells and induces IL-10 secretion via activated STAT1 and STAT3 | [151] | |
Monocyte | Alter monocytic ROS production and mitochondrial ETC-related genes | ||
Dimethyl fumarate (DMF) | CD4 or CD8 | Increase caspase-mediated apoptosis through CytC, reduce intracellular GSH, increase MMP, ROS levels and mitochondrial OCR | [104] |
Tc17 | Upregulate ROS in Tc17 cells through PI3K-AKT-T-BET and IL-2-STAT5 signaling pathways | [105] | |
Monocyte | Upregulate monocytic ROS production as a result of genetically sustained low level of the promotor methylation of NOX3 | [120] | |
Mϕ | Inhibit glycolysis process and ROS production through decreasing ERK phosphorylation | [124] | |
DC | Regulate oxidative stress potentially through modulation GSH-HO-1 pathway | ||
Teriflunomide | T cell | Enhance OCR and EACR by boosting complex III activity in the ETC | [78] |