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Updated: Jul 9, 2026

Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice
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Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice

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TRAIL-R deficiency in mice promotes susceptibility to chronic inflammation and tumorigenesis

Niklas Finnberg1, Andres J P Klein-Szanto, Wafik S El-Deiry

  • 1Laboratory of Molecular Oncology and Cell Cycle Regulation, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA.

The Journal of Clinical Investigation
|December 15, 2007
PubMed

Insights

The TNF-related apoptosis-inducing ligand receptor (TRAIL-R) acts as a crucial tumor suppressor. Loss of TRAIL-R in mice led to increased tumor development, metastasis, and reduced survival, highlighting its role in preventing cancer.

Area of Science:

  • Immunology
  • Oncology
  • Molecular Biology

Background:

  • Preclinical studies suggest TRAIL death-signaling receptors are potential cancer therapy targets.
  • The in vivo role of these receptors in suppressing tumor emergence and growth remains unclear.

Purpose of the Study:

  • To investigate the function of TNF-related apoptosis-inducing ligand receptor (TRAIL-R) as a tumor suppressor in vivo.
  • To determine if TRAIL-R deficiency impacts lymphoma development, metastasis, and response to radiation or chemical carcinogens.

Main Methods:

  • Utilized Emu-myc mice with TRAIL-R allele loss to study lymphoma development.
  • Assessed survival and tumor formation in TRAIL-R knockout mice after sublethal irradiation and diethylnitrosamine (DEN) treatment.
  • Histological analysis and NF-kappaB p65 expression were evaluated.

Main Results:

  • Loss of TRAIL-R significantly reduced lymphoma-free survival and increased metastatic potential.
  • TRAIL-R deficiency led to apoptotic defects in lymphomas and decreased survival after irradiation.
  • TRAIL-R knockout mice exhibited increased susceptibility to DEN-induced hepatocarcinogenesis with larger tumors and apoptotic defects.

Conclusions:

  • TRAIL-R functions as an in vivo suppressor of inflammation and tumor development.
  • TRAIL-R deficiency promotes tumorigenesis and metastasis across multiple tissues.
  • TRAIL-R is a critical regulator of apoptosis and immune response in cancer suppression.

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