Interleukin-35 Gene-Modified Mesenchymal Stem Cells Protect Concanavalin A-Induced Fulminant Hepatitis by Decreasing the Interferon Gamma Level

Hum Gene Ther. 2018 Feb;29(2):234-241. doi: 10.1089/hum.2017.171. Epub 2017 Oct 20.

Abstract

Interleukin 35 (IL-35) is a relatively newly identified cytokine required for the regulatory and suppressive functions of regulatory T cells (Treg), playing an important role in the prevention of autoimmune diseases. This study used mesenchymal stem cells (MSCs) as the gene-delivery vehicles for IL-35 gene therapy and investigated their protective effects in Concanavalin A (Con A)-induced autoimmune hepatitis. Results showed that IL-35 gene modified MSCs (IL-35-MSCs) can specifically migrate to the injured liver tissues and significantly narrow the necrosis areas of injured livers. IL-35-MSCs prevented hepatocyte apoptosis by reducing the FASL expression by mononuclear cells. Although MSC treatment can alleviate liver injury to some extent, IL-35-MSCs showed a stronger protective effect, which means some novel mechanisms exist. The results show that IL-35-MSCs could decrease the level of interferon gamma secreted by liver mononuclear cells through the JAK1-STAT1/STAT4 signal pathway. In summary, this study thus demonstrates a novel and efficient treatment for Con A-induced fulminant hepatitis through negatively regulating the secretion of interferon gamma, thus providing a novel therapeutic approach for this devastating liver disease.

Keywords: interferon gamma; interleukin-35; liver injury; mesenchymal stem cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / genetics
  • Concanavalin A / toxicity
  • Fas Ligand Protein
  • Gene Expression Regulation / genetics
  • Gene Transfer Techniques
  • Hepatitis, Autoimmune / etiology
  • Hepatitis, Autoimmune / genetics*
  • Hepatitis, Autoimmune / therapy
  • Hepatocytes / metabolism
  • Hepatocytes / pathology
  • Humans
  • Interferon-gamma / genetics*
  • Interleukins / genetics*
  • Interleukins / therapeutic use
  • Janus Kinase 1 / genetics
  • Liver / metabolism
  • Liver / pathology
  • Liver Failure, Acute / chemically induced
  • Liver Failure, Acute / genetics
  • Liver Failure, Acute / pathology
  • Liver Failure, Acute / therapy*
  • Male
  • Mesenchymal Stem Cell Transplantation*
  • Mesenchymal Stem Cells / cytology
  • Mice
  • T-Lymphocytes, Regulatory / metabolism
  • T-Lymphocytes, Regulatory / pathology

Substances

  • FASLG protein, human
  • Fas Ligand Protein
  • Interleukins
  • interleukin-35, human
  • Concanavalin A
  • Interferon-gamma
  • Janus Kinase 1