Related Experiment Video

Updated: Aug 14, 2026

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c
07:42

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c

Published on: June 29, 2011

Glucocorticoid hormones in the regulation of cell death

C Riccardi1, O Zollo, G Nocentini

  • 1Dept. of Clinical and Experimental Medicine, University of Perugia, Italy.

Therapie
|June 22, 2000
PubMed

Insights

Glucocorticoids (GCH) regulate T-cell apoptosis via the novel gene GILZ. GILZ inhibits T-cell activation and programmed cell death, suggesting anti-inflammatory and immunosuppressive effects.

Area of Science:

  • Immunology
  • Molecular Biology
  • Cell Biology

Background:

  • T-cell responses are regulated by programmed cell death (PCD), also known as lymphocyte apoptosis.
  • Gene expression, including cytokines (IL-2/IL-2R) and transcription factors (NF-kB), controls T-cell activation and apoptosis.
  • NF-kB exhibits a dual role, activating both cell suicide and anti-death programs.

Purpose of the Study:

  • To investigate the mechanism of GCH-mediated inhibition of T-cell death and activation.
  • To identify the role of the newly discovered gene GILZ in this process.

Main Methods:

  • Transfected cells were used to study GILZ overexpression.
  • Assessed the impact of GILZ on NF-kB/DNA-binding activity, IL-2 production, IL-2R expression, and Fas/FasL complex transcription following TCR triggering.

Main Results:

  • GILZ overexpression inhibited NF-kB/DNA-binding activity.
  • GILZ suppressed IL-2 production and IL-2R expression.
  • GILZ reduced the transcription of the Fas/FasL complex, crucial for T-lymphocyte apoptosis.

Conclusions:

  • GILZ represents a novel mechanism for GCH-mediated inhibition of T-cell death and activation.
  • The findings suggest GILZ's potential contribution to anti-inflammatory and immunosuppressive therapies.

More Related Videos

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death09:18

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Published on: December 27, 2016

LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation06:12

LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation

Published on: May 3, 2024

Related Concept Videos

Overview of Cell Death01:30

Overview of Cell Death

Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the 20th century...
Apoptosis01:30

Apoptosis

Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size reduction of the tissue.
Caspases01:24

Caspases

Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside cells.
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
Regulation of Hematopoietic Stem Cells01:01

Regulation of Hematopoietic Stem Cells

All blood and immune cells are produced from the multipotent hematopoietic stem cells (HSCs) by the process of hematopoiesis. However, they all have a limited life span. In addition, many are depleted in immune surveillance or combatting an injury or infection. This makes blood one of the most regenerative tissues. Hematopoiesis helps replenish these blood and immune cells, restoring the body's normal functioning. However, overproduction of blood and immune cells can make them cancerous or...
Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...