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Baker LD, Espeland MA, Whitmer RA, Snyder HM, Leng X, Lovato L, et al

Autoimmun Rev (2019) 18(2):13743

In conclusion, we show that APAP toxicity in HepG2 cells is largely independent of oxidative stress, and is linked instead to a decoupling of glycolysis from the TCA cycle, lactic acidosis, reduced NADPH production, and subsequent suppression of the anabolic pathways required for rapid growth

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This pattern suggests the important role of early recall responses of T cells and non-nAbs in protection from severe disease [63, 64]