Table 1 Mechanisms of mitochondrial and metabolic dysfunction that influence T cell function

Bcl2, OPA1, PHB2, SIRT3, OMA1 and ATG5 regulate mitochondria-mediated death

Regulate apoptosis of T cells

[29, 68,69,70,71,72]

Increase aldolase, HK-1, ENO1, GLUT1, DLAT and DLST, glycolysis and mitochondrial respiration activity via IFN beta treatment

Restore T cell metabolic remodeling

[77]

Increase oxygen consumption rate (OCR) and extracellular acidification rate (ECAR) through enhancing complex III activity of the ETC after teriflunomide treatment

Prevent the proliferation of T cells

[78]

Reduction in the superoxide dismutase (SOD) and glutathione peroxidase (GPX), as well as an increase in the protein Hsp70 caused by oxidative stress, lead to increase GLUT1 and lactate

Regulate CD4⁺ T cell metabolic reprogramming

[75]

ROS-driven activation of TGF-β signaling in CD4⁺ T cells

Encourage the differentiation of Th17 cells

[80]

MitoTEMPO inhibits ROS in Treg

Decline Th1 and Th17 cells differentiation

[81]

Oleic acid enhances fatty acid β-oxidation of Treg

Enhance inhibition of tissue-resident Treg

[86]

Upregulated mTOR activity increases acetyl-CoA levels and glucose oxidation by pentanoate

Increase IL-10 secretion and suppress IL-17A production in CD4⁺ T cells

[87,88,89]

Phospholipids (PLs) suppress phosphorylation of Bim and Bad molecules

Inhibit the activation and promotion apoptosis of autoreactive CD4⁺ T cells

[90]

Acetyl-CoA carboxylase 1 (ACC1) promotes de novo fatty acid production and the glycolytic-lipogenic pathway

Increase IFN-γ⁺ Th17 cells number and decrease FOXP3⁺ Tregs number in the spinal cord

[91]

Atorvastatin induces p-STAT6, inhibits p-STAT4 expression and cholesterol synthesis

Promote Th2 cells differentiation, inhibit Th1 and Th 17 cells differentiation

[92]

Inhibit PFKFB3-HIF1α activation

Decline Th17 cells differentiation

[94]

Decrease transcription factor TF-like (BATF) expression and upregulate ATP-linked oxidative phosphorylation (OXPHOS)

Promote Th17 cells differentiation and increase the chromatin accessibility

[95, 96]

Linezolid disrupts the integrity of the ETC by inhibiting mitochondrial elongation factor G1 (mEF-G1) and the ratio of NAD⁺/NADH

Promote Th17 and Th1 cells differentiation

[97]

Pik3c3-deficient CD4⁺ T downregulation of ECAR and OCR

Inhibit Th1 cells differentiation

[98]

Nur77 knock-out enhances OCR and EACR

Promote Th1 and Th17 cells differentiation

[99]

2-DG treatment in CD8⁺ T cells reduces CD69 and CD25

Decrease CD8⁺ T cells activation and TNF α production

[103]

DMF reduces intracellular GSH, CytC and induces ROS, mitochondrial membrane potential (MMP), OCR and caspase-mediated apoptosis

Increase apoptosis of CD4⁺ T cells and CD8⁺ T cells

[104]

DMF increases ROS in Tc17 cells through PI3K-AKT-T-BET and IL-2-STAT5 signaling pathways

Decrease IL-17 production in Tc17 cells and inhibit type I or II histone deacetylases (HDACs) histone acetylation on the Il17 locus

[105]