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In-vitro Mutagenesis01:16

In-vitro Mutagenesis

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To learn more about the function of a gene, researchers can observe what happens when the gene is inactivated or “knocked out,” by creating genetically engineered knockout animals. Knockout mice have been particularly useful as models for human diseases such as cancer, Parkinson’s disease, and diabetes.
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Related Experiment Video

Updated: Aug 7, 2025

A Phenotyping Regimen for Genetically Modified Mice Used to Study Genes Implicated in Human Diseases of Aging
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A Phenotyping Regimen for Genetically Modified Mice Used to Study Genes Implicated in Human Diseases of Aging

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Immune Phenotypic Characterization of a TRAIL-Knockout Mouse.

Ani K Stoyanova1, Arne Sattler1, Elisabeth M Hahn1

  • 1Department of General, Visceral and Vascular Surgery, Campus Benjamin Franklin, Charité-Universitätsmedizin Berlin, Hindenburgdamm 30, 12203 Berlin, Germany.

Cancers
|March 11, 2023
PubMed
Summary

Mice lacking TNF-related apoptosis-inducing ligand (TRAIL) showed altered immune cell distribution and function, impacting T-cell proliferation and regulatory T-cell (Treg) suppressiveness, offering insights into TRAIL-based cancer therapies.

Keywords:
TRAIL: immunological phenotypedendritic cellsknockout mouselymphocytes

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Area of Science:

  • Immunology
  • Cancer Biology
  • Molecular Medicine

Background:

  • Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) targets tumor cells but faces clinical challenges due to resistance.
  • TRAIL influences the immune system, affecting tumor growth and therapeutic outcomes.
  • Previous studies indicated improved survival in TRAIL-deficient mice with pancreatic cancer.

Purpose of the Study:

  • To comprehensively characterize the immunological landscape of TRAIL-deficient (TRAIL-/-) mice.
  • To investigate the impact of TRAIL deficiency on immune cell populations and functions.
  • To establish a foundation for future research on TRAIL's role in immunology and cancer therapy.

Main Methods:

  • Flow cytometry analysis of T-cell subsets (CD3+, CD4+, CD8+, Tregs, memory cells) and dendritic cells.
  • Assessment of T-lymphocyte proliferation rates in response to TRAIL.
  • Evaluation of regulatory T-cell (Treg) suppressive function.
  • Comparison of immune cell distribution between TRAIL-/- and wild-type mice.

Main Results:

  • No significant differences in CD3+, CD4+, CD8+, Tregs, or central memory T-cells were observed.
  • Significant alterations were found in effector memory T-cells, CD8+CD122+ cells, and dendritic cell populations.
  • TRAIL-/- T-lymphocytes exhibited lower proliferation rates, which were increased by recombinant TRAIL.
  • Regulatory T-cells from TRAIL-/- mice showed reduced suppressive activity.
  • TRAIL-/- mice displayed an increased proportion of type-2 conventional dendritic cells (DC2s).

Conclusions:

  • TRAIL deficiency leads to distinct changes in the distribution and function of specific immune cell subsets, including T-cells and dendritic cells.
  • These immunological alterations in TRAIL-/- mice provide a basis for understanding TRAIL's complex role in immunity and cancer.
  • The findings suggest potential immunomodulatory strategies involving TRAIL for cancer treatment.