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. Author manuscript; available in PMC: 2020 Apr 1.
Published in final edited form as: Immunometabolism. 2020 Feb 10;2(2):e200009. doi: 10.20900/immunometab20200009

Table 1.

Potential therapeutic target of metabolic pathway in SLE.

Therapeutic target Therapy Effect on T cells Effects on SLE
Hexokinase and mitochondrial complex I 2-deoxy-d glucose and metformin Decrease IFNγ production and decreases Tfh cells Reduces disease activity, and improve kidney disease
Glutaminase 1 BPTES, CB-839, and 968 Reduces Th17 cell differentiation Reduces disease activity, and improve kidney disease
Mitochondrial metabolism Bz-423 Promotes autoreactive T cell apoptosis Reduces disease activity
Glucosylceramide synthetase NB-DNJ Normalizes TCR signaling and restores BTLA expression Reduces disease activity
Cysteine metabolism N-acetyl cysteine Inhibits mTOR activity Reduces disease activity, and improve kidney disease
mTOR signaling Sirolimus Inhibits Th17 differentiation and promotes Treg differentiation Reduces disease activity
PPARγ Pioglitazone (agonist) Promotes Treg expansion Improves nephritis

BTLA, B and T lymphocyte attenuator; BPTES, bis-2-(5-phenylacetamido-1,3,4-thiadiazol-2-yl)ethyl sulfide; mTOR, mammalian target of rapamycin; PPARγ, peroxisome proliferator-activated receptor γ; Tfh, follicular helper T cells.