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The anti-inflammatory IFITM genes ameliorate colitis and partially protect from tumorigenesis by changing immunity

Zoya Alteber1, Adi Sharbi-Yunger1, Meirav Pevsner-Fischer1

  • 1Department of Immunology, The Weizmann Institute of Science, Rehovot, 76100, Israel.

Immunology and Cell Biology
|January 23, 2018
PubMed

Insights

Interferon inducible transmembrane (IFITM) genes are crucial for maintaining gut health and preventing colon cancer. Loss of IFITM genes exacerbates inflammation and promotes tumor development, highlighting their therapeutic potential.

Area of Science:

  • Gastroenterology
  • Immunology
  • Oncology

Background:

  • Inflammation is integral to tumor progression.
  • Interferon inducible transmembrane (IFITM) genes are implicated in gastrointestinal diseases.
  • Understanding gene-host interactions is key for cancer therapy.

Purpose of the Study:

  • To investigate the role of IFITM3 in colonic homeostasis, inflammation, and colitis-associated tumorigenesis.
  • To determine the hematopoietic contribution to colitis severity.
  • To explore the impact of IFITM gene deficiency on gut microbiota.

Main Methods:

  • Utilized IFITM3-deficient mice models.
  • Induced colitis chemically and assessed disease severity.
  • Performed bone marrow transplantation experiments.
  • Analyzed cytokine expression profiles (Th17, IL-10).
  • Sequenced 16S rRNA to characterize gut microbiota.

Main Results:

  • IFITM3 deficiency significantly worsened colitis and promoted invasive tumorigenesis.
  • Hematopoietic cells were identified as key drivers of colitis severity.
  • Lack of IFITM genes led to a pro-inflammatory Th17 response and reduced IL-10 during recovery.
  • Mice lacking the entire IFITM locus spontaneously developed chronic colitis.
  • Significant alterations in gut bacterial composition were observed in IFITM-deficient mice.

Conclusions:

  • IFITM genes play a critical protective role in ameliorating colitis and associated tumorigenesis.
  • IFITM deficiency disrupts immune homeostasis and promotes a pathogenic inflammatory environment.
  • Targeting IFITM genes may offer novel therapeutic strategies for inflammatory bowel disease and colorectal cancer.
Keywords:
Inflammatory bowel diseaseT helper 1 cellsT helper 17 cellsimmune disordersmicrobiometumor immunology

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