Role of interleukin-22 in the development and progression of liver fibrosis
10.3969/j.issn.1001-5256.2021.12.039
- VernacularTitle:IL-22在肝纤维化发生发展中的作用
- Author:
Yuxi MENG
1
;
Lijuan HUO
2
Author Information
1. Department of Gastroenterology, The Second Hospital Affiliated to Shanxi Medical University, Taiyuan 030001, China
2. Department of Gastroenterology, The First Hospital Affiliated to Shanxi Medical University, Taiyuan 030001, China
- Publication Type:Reviews
- Keywords:
Liver Cirrhosis;
Interleukin-22;
Pathologic Processes
- From:
Journal of Clinical Hepatology
2021;37(12):2924-2927
- CountryChina
- Language:Chinese
-
Abstract:
Liver fibrosis is the result of persistent inflammatory response and chronic scar healing response during chronic liver injury and may progress to liver cirrhosis, portal hypertension, and liver failure, which finally requires liver transplantation. Interleukin-22 (IL-22) belongs to the IL-10 family and is the only cytokine that is produced by immune cells but does not act on immune cells. IL-22 plays a role by binding to its receptors IL-22R1 and IL-10R2, which has attracted much attention in the field of liver disease research in recent years. IL-22 not only plays the role of anti-inflammation and promotion of liver regeneration and tissue repair, but also has a pro-inflammatory effect in liver diseases, and it exerts a protective effect on the liver by reducing fibrosis in some pathological conditions, but there are still controversies over its association with liver fibrosis. IL-22 has different effects and mechanisms in liver fibrosis caused by different etiologies. This article reviews the role and possible mechanisms of IL-22 in liver fibrosis caused by viral infection (HBV and HCV), alcohol, high-fat diet, and autoimmunity.
