Hepatic interleukin-7 expression regulates T cell responses

Immunity. 2009 Mar 20;30(3):447-57. doi: 10.1016/j.immuni.2009.01.007. Epub 2009 Mar 12.


Systemic cytokine activity in response to Toll-like receptor (TLR) signaling induces the expression of various proteins in the liver after infections. Here we show that Interleukin-7 (IL-7), the production of which was thought to occur at a constant rate in vivo, was a hepatically expressed protein that directly controled T cell responses. Depletion of IL-7 expression in the liver abrogated several TLR-mediated T cell events, including enhanced CD4+ T cell and CD8+ T cell survival, augmented CD8+ T cell cytotoxic activity, and the development of experimental autoimmune encephalitis, a Th17 cell-mediated autoimmune disease. Thus, T cell responses are regulated by hepatocyte-derived IL-7, which is expressed in response to TLR signaling in vivo. We suggested that TLR-induced IL-7 expression in the liver, which is an acute-phase response, may be a good diagnostic and therapeutic target for efficient vaccine developments and for conditions characterized by TLR-mediated T cell dysregulation, including autoimmune diseases.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cells, Cultured
  • Enzyme-Linked Immunosorbent Assay
  • Flow Cytometry
  • Gene Expression Regulation / drug effects
  • Hepatocytes / immunology
  • Interleukin-7 / metabolism*
  • Lipopolysaccharides / pharmacology
  • Liver / immunology*
  • Mice
  • Mice, Inbred C57BL
  • Polymerase Chain Reaction
  • T-Lymphocytes / immunology*


  • Interleukin-7
  • Lipopolysaccharides