Related Experiment Video

Updated: Aug 20, 2026

Assessment of the Synaptic Interface of Primary Human T Cells from Peripheral Blood and Lymphoid Tissue
06:27

Assessment of the Synaptic Interface of Primary Human T Cells from Peripheral Blood and Lymphoid Tissue

Published on: July 30, 2018

Galectin-1 sensitizes resting human T lymphocytes to Fas (CD95)-mediated cell death via mitochondrial

Paola Matarrese1, Antonella Tinari, Elisabetta Mormone

  • 1Department of Drug Research and Evaluation, and Technology and Health, Istituto Superiore di Sanità, Viale Regina Elena, 299, Rome 00161, Italy.

The Journal of Biological Chemistry
|November 24, 2004
PubMed

Insights

Galectin-1 (Gal-1) sensitizes human T cells to Fas-mediated apoptosis. This protein induces mitochondrial changes, impacting cell death pathways relevant to cancer and inflammation.

Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Medicine

Background:

  • Galectins are immunoregulatory proteins crucial for T cell homeostasis.
  • Galectin-1 (Gal-1) is implicated in tumor-immune escape by inducing effector T cell death.

Purpose of the Study:

  • To investigate the role of Gal-1 in T cell apoptosis.
  • To elucidate the molecular mechanisms underlying Gal-1-induced T cell death.

Main Methods:

  • Studied the effect of Gal-1 on human resting T cells.
  • Analyzed Fas/caspase-8-mediated cell death pathways.
  • Investigated mitochondrial membrane potential, ceramide pathway, and mitochondrial dynamics (h-Fis, DRP-1).

Main Results:

  • Gal-1 sensitizes human T cells to Fas/caspase-8-mediated apoptosis.
  • Gal-1 triggers apoptosis via mitochondrial membrane potential increase and the ceramide pathway.
  • Gal-1 induces significant changes in mitochondrial morphology and dynamics.

Conclusions:

  • Gal-1 induces T cell death through a novel pathway involving Fas and mitochondria.
  • Gal-1-induced mitochondrial morphogenetic changes offer a model for studying cell death execution.
  • This study provides a mechanistic basis for Gal-1's immunoregulatory roles in cancer and inflammation.

More Related Videos

Measuring Composition of CD95 Death-Inducing Signaling Complex and Processing of Procaspase-8 in this Complex07:17

Measuring Composition of CD95 Death-Inducing Signaling Complex and Processing of Procaspase-8 in this Complex

Published on: August 2, 2021

A GPC3-targeting Bispecific Antibody, GPC3-S-Fab, with Potent Cytotoxicity11:13

A GPC3-targeting Bispecific Antibody, GPC3-S-Fab, with Potent Cytotoxicity

Published on: July 12, 2018

Related Concept Videos

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...
Autophagic Cell Death01:18

Autophagic Cell Death

Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and pro-apoptotic...
GPCR Desensitization01:12

GPCR Desensitization

G protein-coupled receptor (GPCR) signaling plays a crucial role in cell functioning. GPCR desensitization is an equally essential process. It allows cells to respond to changing environments and regain sensitivity to new stimuli while preventing unnecessary stimulation when no longer needed. Prolonged exposure to stimuli leads to GPCR desensitization. It involves blocking the receptors from binding and activating additional G proteins. This inhibits activation of downstream effectors, thereby...
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...
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...
Phagocytosis of Apoptotic Cells01:17

Phagocytosis of Apoptotic Cells

Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or  immature dendritic cells. Non-professional phagocytes such as  epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes. 
Normal cells contain receptors that prevent them from being recognized by phagocytes.