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白细胞介素-22 如何介导肝再生并预防损伤和纤维化?

How Does Interleukin-22 Mediate Liver Regeneration and Prevent Injury and Fibrosis?

机构信息

Cell & Molecular Biology Lab, Department of Zoology, University of the Punjab, Lahore, Pakistan.

Centennial College, Scarborough, Toronto, ON, Canada.

出版信息

J Immunol Res. 2016;2016:2148129. doi: 10.1155/2016/2148129. Epub 2016 Dec 6.

DOI:10.1155/2016/2148129
PMID:28050571
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5168458/
Abstract

Interleukin-22 (IL-22) is a pluripotent T cell-derived cytokine which is a member of IL-10 cytokine family. It is the only interleukin produced by immune cells but does not target immune system components. IL-22 is mainly produced by dendritic cells (DCs) and TH17, TH22, NK, and NKT cells and targets a number of body tissues including liver, pancreas, and other epithelial tissues. It provokes a series of downstream signaling pathways upon binding with IL-22R complex which protects liver damage through STAT3 activation. IL-22BP is an inhibitor of IL-22 which has 20-1000x more affinity to bind with IL-22 compared to IL-22R1 that inhibits IL-22 activity. Its level was found to be positively correlated with the severity of liver damage and fibrosis. So, the present review is an effort to reveal the exact mechanism lying in the hepatoprotective activity of IL-22 and some of its future therapeutic implications.

摘要

白细胞介素-22(IL-22)是一种多功能 T 细胞衍生的细胞因子,属于白细胞介素 10 细胞因子家族。它是免疫细胞产生的唯一一种白细胞介素,但不针对免疫系统成分。IL-22 主要由树突状细胞(DCs)和 TH17、TH22、NK 和 NKT 细胞产生,作用于包括肝脏、胰腺和其他上皮组织在内的多种身体组织。它与 IL-22R 复合物结合后,会引发一系列下游信号通路,通过激活 STAT3 来保护肝脏免受损伤。IL-22BP 是 IL-22 的抑制剂,与 IL-22R1 相比,它与 IL-22 的结合亲和力高 20-1000 倍,从而抑制 IL-22 的活性。其水平与肝损伤和纤维化的严重程度呈正相关。因此,本综述旨在揭示 IL-22 的肝保护活性的确切机制及其一些潜在的治疗意义。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c29/5168458/aef53a8077ce/JIR2016-2148129.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c29/5168458/4a9ab6f5fe91/JIR2016-2148129.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c29/5168458/aef53a8077ce/JIR2016-2148129.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c29/5168458/4a9ab6f5fe91/JIR2016-2148129.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c29/5168458/aef53a8077ce/JIR2016-2148129.002.jpg

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