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The KCH in London, United Kingdom developed a prognostic model based on two groups of patients, those with APAP-induced acute liver failure and those with non-APAP-induced acute liver failure

Although their precise mechanisms of action remain to be completely elucidated, it has been reported that HCQ inhibits the mitochondrial antioxidant system induced by TCR crosslinking, consequently increasing mROS levels and reducing CD4+ T cell proliferation through oxidative stress (173)