Table 1.

The dual role of immune cells in AILI.

	Proinflammatory	No Effect or Pro-Regenerative
Neutrophils	Depleted neutrophils could protect against AILI via reduced FasL-expression, hepatocytotoxicity, and mitochondrial respiratory chain burst [32]. Blockade of neutrophil infiltration by anti-granulocyte receptor 1 depletion or combined CXCR2-FPR1 antagonism prevented liver injury [46]	No activation of circulating and liver neutrophils during AILI [42]. Neutrophil infiltration could be moving necrotic cell debris but not cause further damage, and CD-18-deficient mice were not protected [43]. gp91phox−/− did not protect [44]. Anti-Ly6G, genetic knockout in granulocyte-colony-stimulating factor, or genetic deletion in Nox2 did not protect against APAP overdose, promoting the phenotypic conversion of proinflammatory macrophages to pro-resolving macrophages, and promoting liver repair [45]
KCs	Depletion of KCs can restrain APAP injury [50,51]. Mincle deletion (or KCs depletion) may reduce APAP hepatotoxicity [52].	EPO promotes the proliferation and function of KCs, ameliorating AILI [53]. Depletion of KCs can lead to liver injury aggravation [54,55,56]. KCs against AILI by secreting cytokines [57,58,59,60]
MoMFs	The activated MoMFs produce O2.-, NO., and peroxynitrite, promoting AILI progression [51], and upregulating proinflammatory gene expressions [61,62].	Upregulate endocytosis- and apoptotic-cell-clearance-related proteins which promote liver repair [63]. Promotes macrophage differentiation [64,65,66,67].
DCs		Prevent NKs cell activation and induce neutrophil apoptosis to reveal a protective role [68].
NK/NKT cells	Amplified the immune response, upregulated proinflammatory cytokine expressions, and increased neutrophil accumulation [41]. DMSO activated NK/NKT cells [69]. NKT-cell-deficient (Jα18−/−) mice could be resistant to AILI [70].	NKT cell-deficient mice (CD1d−/− and Jα18−/−) were more vulnerable to AILI [71]. Reduce the release of inflammatory cytokines [72].
γδT cells	Depletion of γδT cells reduced IL-17A production and attenuated liver injury [34]. HIF attenuated abnormal γδT cell recruitment and alleviated AILI [73].

HIF—hypoxia-inducible factor-1; Nox2—NADPH oxidase 2; APAP—acetyl-para-aminophenol; AILI—APAP-induced liver injury; EPO—erythropoietin; KCs—Kupffer cells; MoMFs—monocyte-derived macrophages; DCs—dendritic cells; NK/NKT cells—natural killer cells and NKT cells; DMSO—dimethyl sulfoxide; IL—interleukin.