Related Experiment Video
Updated: Aug 15, 2026

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes
Published on: September 26, 2013
Role of cytokines in autoimmunity
1Department of Pathology, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02115, USA.
Abstract:
Activation-induced apoptosis of T lymphocytes is an important mechanism for maintaining self-tolerance. The sensitivity of T cells to apoptosis by the Fas pathway is regulated by the exposure of these cells to different cytokines. IL-2 is a survival and growth factor for T cells, as well as a necessary potentiator of Fas-mediated cell death. The role of this cytokine in triggering death pathways is the likely explanation for the autoimmune disease that develops as a result of targeted disruption of the IL-2 or IL-2 receptor alpha or beta chain gene.
More Related Videos
08:47Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues
Published on: May 8, 2016
12:36Single-cell Analysis of Immunophenotype and Cytokine Production in Peripheral Whole Blood via Mass Cytometry
Published on: June 26, 2018
Related Concept Videos
The JAK-STAT Signaling Pathway
Inflammatory Response
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
T Cell Types and Functions
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
Immune Response Against Viral Pathogens
NK Cells
NK cells are a crucial part of our innate immune system, acting as the first line of defense against viral infections. These cells can recognize and kill infected cells without prior exposure to the virus, effectively slowing down the spread of infection. Additionally, NK cells produce proinflammatory...
Autoimmune Disorders
Concept and Mechanism of Autoimmune Diseases
The immune system...
Type I Diabetes II: Pathophysiology