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Related Concept Videos

Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
T Cell Activation and Clonal Selection01:22

T Cell Activation and Clonal Selection

T cells are integral to our adaptive immune system, recognizing and effectively responding to foreign antigens. T cell activation and clonal selection are pivotal in orchestrating this immune response. This article elucidates these mechanisms, detailing the roles of cluster of differentiation (CD) markers, major histocompatibility complex (MHC) molecules, costimulatory signals, and the process of clonal selection.
Naive T cells that have not yet encountered an antigen express two primary CD...
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
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Related Experiment Video

Updated: May 22, 2026

Tailoring In Vivo Cytotoxicity Assays to Study Immunodominance in Tumor-specific CD8+ T Cell Responses
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Tailoring In Vivo Cytotoxicity Assays to Study Immunodominance in Tumor-specific CD8+ T Cell Responses

Published on: May 6, 2019

Conditional IL-2 Gene Deletion: Consequences for T Cell Proliferation.

Zoran Popmihajlov1, Dong Xu, Heather Morgan

  • 1Division of Immunology, Department of Medicine, Weill Cornell Medical College New York, NY, USA.

Frontiers in Immunology
|May 17, 2012
PubMed
Summary

Interleukin-2 (IL-2) is not solely responsible for T cell blastogenesis, but drives aerobic glycolysis. Proliferation depends on gamma-chain cytokines, not just CD3/CD28 activation, in this study of conditional IL-2 gene deletion in mice.

Keywords:
T cell proliferationinterleukin-2lymphocyte blastic transformation

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Visualization of IL-22-expressing Lymphocytes Using Reporter Mice
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Visualization of IL-22-expressing Lymphocytes Using Reporter Mice

Published on: January 25, 2017

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Last Updated: May 22, 2026

Tailoring In Vivo Cytotoxicity Assays to Study Immunodominance in Tumor-specific CD8+ T Cell Responses
10:13

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Published on: May 6, 2019

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10:30

Visualization of IL-22-expressing Lymphocytes Using Reporter Mice

Published on: January 25, 2017

Area of Science:

  • Immunology and Molecular Biology
  • Cellular and Immune Response Mechanisms

Background:

  • Interleukin-2 (IL-2) is crucial for T cell development and function.
  • Conventional deletion of the IL-2 gene leads to severe autoimmune disease.
  • Conditional gene deletion strategies are needed to study IL-2's specific roles.

Purpose of the Study:

  • To investigate the precise role of IL-2 in T cell proliferation.
  • To examine IL-2's contribution to aerobic glycolysis and cytokine production.
  • To circumvent the autoimmune issues associated with complete IL-2 deficiency.

Main Methods:

  • Developed a conditional IL-2 gene deletion mouse model using tamoxifen (TAM).
  • Activated splenocytes from wild-type, conventional IL-2 knockout, and conditional knockout mice.
  • Assessed T cell blastogenesis, aerobic glycolysis, DNA synthesis (BrdU), and cell division (CFSE).
  • Quantified IL-2 and other gamma-chain cytokines using ELISA and protein-bead arrays.

Main Results:

  • Conditional IL-2 deficiency (TAM-treated Cre+) mimicked conventional IL-2 deficiency in IL-2 production.
  • T cell blastogenesis occurred in IL-2 sufficient (WT, Cre-, Cre+) but not conventional IL-2 knockout mice.
  • Aerobic glycolysis switch was observed only in IL-2 sufficient T cells.
  • Conditional IL-2 deficiency preserved production of other gamma-chain cytokines, unlike conventional deficiency.

Conclusions:

  • T cell blastogenesis is not solely dependent on IL-2 but requires other gamma-chain cytokines.
  • IL-2 specifically drives the metabolic switch to aerobic glycolysis in activated T cells.
  • Conditional IL-2 deletion provides a model to study IL-2 functions without severe autoimmunity.