Growth differentiation factor-15 suppresses maturation and function of dendritic cells and inhibits tumor-specific immune response

PLoS One. 2013 Nov 13;8(11):e78618. doi: 10.1371/journal.pone.0078618. eCollection 2013.

Abstract

Dendritic cells (DCs) play a key role in the initiation stage of an antigen-specific immune response. A variety of tumor-derived factors (TDFs) can suppress DC maturation and function, resulting in defects in the tumor-specific immune response. To identify unknown TDFs that may suppress DCs maturation and function, we established a high-throughput screening technology based on a human liver tumor T7 phage cDNA library and screened all of the proteins derived from hepatoma cells that potentially interact with immature DCs. Growth/differentiation factor-15 (GDF-15) was detected and chosen for further study. By incubation of DCs cultures with GDF-15, we demonstrate that GDF-15 can inhibit surface protrusion formation during DC maturation; suppress the membrane expression of CD83, CD86 and HLA-DR on DCs; enhance phagocytosis by DCs; reduce IL-12 and elevate TGF-β1 secretion by DCs; inhibit T cell stimulation and cytotoxic T lymphocyte (CTL) activation by DCs. By building tumor-bearing mouse models, we demonstrate that GDF-15 can inhibit the ability of DCs to stimulate a tumor-specific immune response in vivo. These results indicate that GDF-15 may be one of the critical molecules that inhibit DC maturation and function and are involved in tumor immune escape. Thus, GDF-15 may be a novel target in tumor immunotherapy.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Line, Tumor
  • Dendritic Cells / immunology*
  • Granulocyte-Macrophage Colony-Stimulating Factor / physiology
  • Growth Differentiation Factor 15 / physiology*
  • Humans
  • Interleukin-12 / metabolism
  • Lymphocyte Activation
  • Lymphocyte Culture Test, Mixed
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Neoplasm Transplantation
  • Phagocytosis
  • T-Lymphocytes, Cytotoxic / immunology
  • Transforming Growth Factor beta1 / metabolism
  • Tumor Escape*

Substances

  • GDF15 protein, human
  • Growth Differentiation Factor 15
  • TGFB1 protein, human
  • Transforming Growth Factor beta1
  • Interleukin-12
  • Granulocyte-Macrophage Colony-Stimulating Factor

Grants and funding

This work was supported by a grant from the Natural Science Foundation of China (NSFC No 81171978, http://isisn.nsfc.gov.cn/egrantweb). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.