Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

T Cell Types and Functions01:24

T Cell Types and Functions

3.3K
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...
3.3K
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

13.9K
Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
13.9K
Inflammatory Response01:28

Inflammatory Response

18.9K
An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
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,...
18.9K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

12-Lipoxygenase (12-LOX) plays a key role in the hyperinflammatory response caused by SARS-CoV-2.

mBio·2026
Same author

Multi-ancestry polygenic risk scores for the prediction of type 2 diabetes and complications in diverse ancestries.

medRxiv : the preprint server for health sciences·2025
Same author

Effects of Obeticholic Acid Treatment on Primary Human Hepatocytes in a Novel Tri-Culture Model System.

Cells·2025
Same author

Large-scale multi-omics analyses in Hispanic/Latino populations identify genes for cardiometabolic traits.

Nature communications·2025
Same author

12-Lipoxygenase Inhibition Improves Glycemia and Obesity-associated Inflammation in Male Human Gene Replacement Mice.

Endocrinology·2025
Same author

Joint analysis of the nPOD-Virus Group data: the association of enterovirus with type 1 diabetes is supported by multiple markers of infection in pancreas tissue.

Diabetologia·2025

Related Experiment Video

Updated: Mar 30, 2026

Mouse Naïve CD4+ T Cell Isolation and In vitro Differentiation into T Cell Subsets
07:12

Mouse Naïve CD4+ T Cell Isolation and In vitro Differentiation into T Cell Subsets

Published on: April 16, 2015

55.0K

Interleukin-12 (IL-12)/STAT4 Axis Is an Important Element for β-Cell Dysfunction Induced by Inflammatory Cytokines.

Jessica R Weaver1, Jerry L Nadler2,3, David A Taylor-Fishwick1,2,3

  • 1Department of Microbiology and Molecular Cell Biology, Eastern Virginia Medical School, Norfolk, Virginia, United States of America.

Plos One
|November 12, 2015
PubMed
Summary

Inflammation causes beta-cell loss in diabetes. Interleukin-12 (IL-12) and STAT4 signaling mediate this apoptosis, offering potential therapeutic targets for preserving beta-cell function.

More Related Videos

Isolated Pancreatic Islet Treatment and Apoptosis Measurement
09:36

Isolated Pancreatic Islet Treatment and Apoptosis Measurement

Published on: May 2, 2025

1.0K
Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes
12:59

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes

Published on: September 26, 2013

35.7K

Related Experiment Videos

Last Updated: Mar 30, 2026

Mouse Naïve CD4+ T Cell Isolation and In vitro Differentiation into T Cell Subsets
07:12

Mouse Naïve CD4+ T Cell Isolation and In vitro Differentiation into T Cell Subsets

Published on: April 16, 2015

55.0K
Isolated Pancreatic Islet Treatment and Apoptosis Measurement
09:36

Isolated Pancreatic Islet Treatment and Apoptosis Measurement

Published on: May 2, 2025

1.0K
Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes
12:59

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes

Published on: September 26, 2013

35.7K

Area of Science:

  • Immunology
  • Endocrinology
  • Cell Biology

Background:

  • Diabetes pathology involves beta-cell loss, often linked to chronic inflammation.
  • Inflammatory cytokines like IL-1β, TNF-α, and IFN-γ impair beta-cell function and viability.
  • The precise mechanisms of cytokine-induced beta-cell apoptosis remain unclear.

Purpose of the Study:

  • To elucidate the role of specific cytokines and signaling pathways in inflammation-driven beta-cell apoptosis.
  • To identify key mediators contributing to beta-cell loss in diabetic conditions.
  • To explore potential therapeutic targets for preserving beta-cell function.

Main Methods:

  • In vitro exposure of beta-cells and islets to cytokine cocktails (IL-1β/TNF-α/IFN-γ).
  • Evaluation of individual and combined cytokine effects on cell apoptosis.
  • Analysis of interleukin-12 (IL-12) expression and its signaling axis (IL-12 receptor, STAT4).
  • Assessment of beta-cell apoptosis in STAT4-deficient mouse islets.

Main Results:

  • Cytokine cooperation, particularly involving IL-1β, is required for beta-cell apoptosis; single cytokines are insufficient.
  • Endogenous IL-12 expression correlates with apoptosis-inducing cytokine combinations.
  • Blocking the IL-12 axis (production, receptor interaction, signaling) protects beta-cells from cytokine-induced apoptosis.
  • STAT4 signaling is implicated, as IL-12 disruption reduces IFN-γ expression.
  • STAT4-deficient islets exhibit resistance to inflammatory cytokine-induced cell death.

Conclusions:

  • Interleukin-12 (IL-12) is a critical mediator of inflammation-induced beta-cell apoptosis.
  • The IL-12/STAT4 signaling pathway plays a significant role in beta-cell death.
  • Modulating IL-12/STAT4 signaling presents a promising therapeutic strategy for preserving beta-cell viability in diabetes.