IL-22在肝纤维化发生发展中的作用

Role of interleukin-22 in the development and progression of liver fibrosis

肝纤维化是慢性肝损伤过程中持续的炎症反应和慢性瘢痕愈合反应的结果。肝纤维化进展可导致肝硬化、门静脉高压和肝衰竭,最终只能进行肝移植。IL-22属于IL-10家族,是目前发现的唯一由免疫细胞产生但不作用于免疫细胞的细胞因子,可通过与其受体IL-22R1/IL-10R2结合而发挥作用,近年来在肝病研究领域中备受关注。IL-22在肝脏疾病中既有抗炎、促进肝再生和组织修复的作用,又有促炎作用。在某些致病条件下,IL-22通过减少纤维化发挥保护肝脏的作用,然而其与肝纤维化的关系目前仍存在争议。对于不同病因引起的肝纤维化,其作用及相关机制也不相同。现就IL-22在病毒感染(HBV、HCV)、酒精、高脂和自身免疫等原因所致肝纤维化中的作用及可能的机制进行综述。

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.