Related Experiment Video

Updated: Aug 25, 2026

Tumor Transplantation for Assessing the Dynamics of Tumor-Infiltrating CD8+ T Cells in Mice
07:36

Tumor Transplantation for Assessing the Dynamics of Tumor-Infiltrating CD8+ T Cells in Mice

Published on: June 12, 2021

Bcl-2 inhibition of T-cell proliferation is related to prolonged T-cell survival

Ningli Cheng1, Yelena M Janumyan, Lisa Didion

  • 1Department of Pathology, The University of Iowa Roy J and Lucille P Carver College of Medicine, 3160 ML, Iowa City, IA 52242, USA.

Oncogene
|March 23, 2004
PubMed

Insights

Bcl-2

Area of Science:

  • Immunology
  • Molecular Biology
  • Cell Biology

Background:

  • The Bcl-2 protein is known to inhibit apoptosis, promoting oncogenesis.
  • Bcl-2 also exhibits antiproliferative effects in certain contexts, but its precise role is debated.
  • The function of Bcl-2 in T-cell proliferation requires further clarification.

Purpose of the Study:

  • To investigate the antiproliferative role of Bcl-2 independently of its anti-apoptotic function.
  • To determine if a mutant Bcl-2 (Bcl-2-Y28A) lacking antiproliferative activity affects T-cell proliferation differently from wild-type Bcl-2.
  • To elucidate the mechanisms by which Bcl-2 influences T-cell proliferation and activation.

Main Methods:

  • Generation of mice expressing a mutant Bcl-2 (Bcl-2-Y28A) lacking reported antiproliferative activity.
  • Comparison of apoptosis inhibition between wild-type (WT) Bcl-2 and Bcl-2-Y28A.
  • Assessment of T-cell proliferation and activation in response to WT-Bcl-2 and Bcl-2-Y28A in T cells from mice of different ages.
  • Analysis of T-cell size, p27 levels, RNA content, and Bax expression in relation to Bcl-2's effects on proliferation.

Main Results:

  • Both WT-Bcl-2 and Bcl-2-Y28A demonstrated similar inhibition of apoptosis.
  • Contrary to expectations based on cell line studies, Bcl-2-Y28A inhibited T-cell proliferation similarly to WT-Bcl-2.
  • Bcl-2 inhibited proliferation of T cells from older animals but not immature ones, correlating with T-cell size and markers of quiescent G0 arrest.
  • Bcl-2's antiproliferative effect was reversed by Bax expression, linked to cell size.

Conclusions:

  • The study does not support genetically distinct roles for Bcl-2 in apoptosis and proliferation.
  • Bcl-2 and Bax appear to regulate T-cell proliferation through modulation of T-cell size and induction of quiescent G0 arrest.
  • These effects are likely a consequence of prolonged T-cell survival mediated by Bcl-2.

More Related Videos

Ex vivo Expansion of Tumor-reactive T Cells by Means of Bryostatin 1/Ionomycin and the Common Gamma Chain Cytokines Formulation07:20

Ex vivo Expansion of Tumor-reactive T Cells by Means of Bryostatin 1/Ionomycin and the Common Gamma Chain Cytokines Formulation

Published on: January 14, 2011

Related Concept Videos

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...
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...
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
B Cell Activation and Differentiation01:24

B Cell Activation and Differentiation

The adaptive immune response, a sophisticated defense mechanism, relies on the activation and differentiation of B lymphocytes, or B cells. These processes enable our bodies to mount a tailored response against specific pathogens such as bacteria, free virus particles, toxins, and parasites.
When naive B cells encounter a specific antigen that can bind to the B cell receptor (BCR) on their surface, they undergo sensitization to respond to the antigen's presence. Sensitization begins with...
T Cell Types and Functions01:24

T Cell Types and Functions

When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
Cytotoxic T Cells-mediated Immune Response01:27

Cytotoxic T Cells-mediated Immune Response

Cytotoxic T cells are a vital component of the immune system. They have the remarkable ability to identify and target antigens on infected or abnormal cells. These antigens often originate from intracellular pathogens such as viruses or abnormal proteins cancer cells produce.
Immunological surveillance is the ability of immune cells to monitor and eliminate infected cells with intracellular pathogens, neoplastically transformed cells, and cells with non-self antigens. Cytotoxic T cells and NK...