Table 6 The impact of mitochondrial and metabolic malfunctioning pathways on the activities of DCs

Sirt6 inhibition potentially mediates metabolic pathways

Reduce migration and activation of DCs

[152, 153]

Knock-out NOX2 in DCs can inhibit T cell-mediated autoimmune neuroinflammation through LC3-associated phagocytosis (LAP)

Inhibit myelin peptide presentation of DCs

[154]

Increased HIF-1α-NDUFA4L2 signaling inhibits X-box binding protein 1 (XBP1) and leads to downregulating OCR and ROS

Promote pro-inflammatory activities and activation of DCs

[155]

Tgfbr2 insufficiency in moDCs upregulates ROS production via NOX2

Secret more IL-12 in moDCs which induces Th1 polarization and chronic inflammatory demyelination

[156]

DMF partly though GSH-HO-1 pathway regulating oxidative stress

Decrease maturation and antigen‐presenting capacity of pro-inflammatory DCs

[157, 160, 161]