Table 2.

The characteristics of the various scientific and intervention studies about IL-22.

Author	System	Approach	Target	Utility for diseases	Reference number
Wei Ren et al.	Lung diseases	Treating with IL-22 and/or AG490	PMVEC apoptosis mediated by AngII through activating the JAK2/STAT3 signaling pathway	Aortic dissection with acute lung injury	45
Minrui Liang et al.	Lung diseases	Administration of recombinant human IL-22	Amelioration of epithelial to mesenchymal transition and partial reversion of the impaired cell viability	bleomycin- induced pulmonary fibrosis	47
Philip L. Simonian et al.	Lung diseases	Preventing expression of IL-22 either by mutating AhR or inhibiting AhR signalling, direct blockade of IL-22 and administration of recombinant IL-22	AhR signaling pathway in γδT cells and recruitment of CD4+T cells to lung	hypersensitivity pneumonitis that progresses to lung fibrosis upon repeated exposure to the ubiquitous microorganism Bacillus subtilis	48
Jill R Johnson et al.	Lung diseases	Injection of IL-22+ TGF-β1	Increased expression of some EMT transcription factors (Snail1 and Zeb1)	Asthma	49
Heather M. McGee et al.	Skin diseases	IL-22−/− mice	IL-22 directs extracellular matrix gene expression as well as myofibroblast differentiation both in vitro and in vivo.	Acute skin wounding repair	50
Geethanjali Pickert et al.	Intestine diseases	STAT3IEC-KO mice	STAT3 regulates the cellular stress response, apoptosis, and pathways associated with wound healing in IECs.	Mucosal wound healing in intestine	28
Caroline A. Lindemans et al.	Intestine diseases	Administration of recombinant IL-22	Recombinant IL-22 directly targeted ISCs, augmenting the growth of both murine and human intestinal organoids, increasing proliferation, and promoting ISC expansion.	Graft vs. host disease in intestine after murine allogeneic bone marrow transplantation	22
Fangchen Gong et al.	Cardiac diseases	Blocking of IL-22R1 with IL-22R1 antibody	IL-22 was found to protect endothelial cells from glucose- and LPC- induced injury.	Type 2 diabetes mellitus and coronary artery disease	4
Yujie Guo et al.	Cardiac diseases	Administration of anti-IL-22 neutralizing antibody	Treatment of acute viral myocarditis and chronic myocarditis mice with an anti-IL-22 Ab decreased the survival rate and exacerbated myocardial fibrosis.	CVB3-induced chronic myocarditis and dilated cardiomyopathy	51
Svetlana Radaeva et al.	Liver diseases	IL-22 blockade with a neutralizing antibody and injection of recombinant IL-22	Blocking STAT3 activation abolishes the antiapoptotic and mitogenic actions in hepatic cells.	T cell-mediated hepatitis induced by concanavalin A	52
Ogyi Park et al.	Liver diseases	Liver-specific IL-22 transgenic mice	Complete resistance to concanavalin A–induced T cell hepatitis with minimal effect on liver inflammation and acceleration of liver regeneration after partial hepatectomy	Concanavalin A–induced T cell hepatitis	53
Zenewicz LA et al.	Liver diseases	IL-22-deficient mice	Protection to hepatocytes injury during acute liver inflammation	Acute liver inflammation	54
Christophe Paget et al.	Infectious	IL-22−/- C57BL/6 mice	DC maturation in response to IAV could lead to IL-22 release by iNKT cells.	Influenza A Virus Infection	55
Qing Kong et al.	Infectious	Administration of anti-IL-22 neutralizing antibody	Anti-IL-22 Antibody decreased the frequencies of Th22 cells and the levels of IL-22, and increased the expressions of cardiac IL-22R1 and neutralization of IL-22 significantly promoted cardiac viral replication.	Coxsackievirus B3-Induced mice acute viral myocarditis	56
Andrea Sommer et al.	Nutrition	Vitamin D treatment of DCs	The differentiation of IL-22-producing T cells mediated by supernatants of vitamin D-treated DCs was dependent on TNF-α IL-6 and IL-23.	– – – –	57
Yong Woo Ji et al.	Eye diseases	IL-22 knock-out mice	IL-22 is essential for suppression of ocular surface infiltration of Th17 cells and inhibition of dry eye disease induction.	Dry eye disease	58
Minling Hu et al.	Autophagy	Administration of recombinant IL-22	Both treatment with IL-22 or 3-MA can partly reverse increased levels of ROS and the overexpression of GRP78 and CHOP induced by Palmitate.	– – – –	59