Dual roles of IL-22 at ischemia-reperfusion injury and acute rejection stages of rat allograft liver transplantation
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Yi Zhang1,2,3,*, Xiaofei Wang4,*, Liwei Mao5,*, Di Yang1, Weiwu Gao1, Zhiqiang Tian1, Mengjie Zhang1, Xia Yang1, Kuansheng Ma4, Yuzhang Wu1 and Bing Ni1,2
1Institute of Immunology, PLA, Third Military Medical University, Chongqing 400038, PR China
2Department of Pathophysiology and High Altitude Pathology, Third Military Medical University, Chongqing 400038, PR China
3Laboratory Department, 150th Hospital of PLA, Luoyang 471031, PR China
4Department of Hepatobiliary Surgery, Southwest Hospital, Third Military Medical University, Chongqing 400038, PR China
5Department of Oncology, 309th Hospital of PLA, Beijing 100091, PR China
*These authors have contributed equally to this work
Bing Ni, email: firstname.lastname@example.org
Yuzhang Wu, email: email@example.com
Kuansheng Ma, email: firstname.lastname@example.org
Keywords: liver transplantation; IL-22; Th17 cells; Treg cells; chemokine
Received: August 16, 2017 Accepted: December 04, 2017 Published: December 15, 2017
Interleukin-22 (IL-22) is a recently identified regulator of inflammation, but little is known about its role in liver transplantation. Therefore, in this study, we explored the roles and the underlying mechanisms of IL-22 in acute allograft rejection by using a rat allogeneic liver transplantation model. Results showed that allograft liver transplantation led to damage of the parent liver and to significantly increased IL-22 expression in the allograft liver and plasma of the recipient rats compared with the rats who received isografts. Moreover, the significantly increased IL-22 expression was accompanied by markedly increased level of phospho-STAT3 in the allogeneic liver tissues after transplantation. Of note, neutralization of the IL-22 protein in recipient rats significantly worsened the function of the allograft liver at 1 day post-transplantation (ischemia-reperfusion injury, IRI) but improved the function at 7 days post-transplantation (acute rejection, AR). At IRI stage, IL-22 protected liver function through the increase of anti-apoptosis and pro-regeneration cytokines. However, IL-22 led to the increase of pro-inflammation factors at AR stage, accompanied by the marked increase of the Th17 and the marked decrease of Treg cells in allograft recipient rats through modulating the expression of chemokines for different cell types, which however were reversed by in vivo IL-22 neutralization. Results indicate the dual roles of IL-22 and suggest the differential potential clinical application of IL-22 at different stage of allograft liver transplantation.
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