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

1.3K
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...
1.3K
B Cell Activation and Differentiation01:24

B Cell Activation and Differentiation

4.3K
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...
4.3K
Cytotoxic T Cells-mediated Immune Response01:27

Cytotoxic T Cells-mediated Immune Response

1.1K
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...
1.1K
cAMP-dependent Protein Kinase Pathways01:25

cAMP-dependent Protein Kinase Pathways

6.5K
Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...
6.5K
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

7.6K
The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
7.6K
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

9.2K
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...
9.2K

You might also read

Related Articles

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

Sort by
Same author

Antigen-presenting cancer-associated fibroblasts in murine pancreatic tumors differentially regulate T-cell phenotype and function.

Journal of immunology (Baltimore, Md. : 1950)·2026
Same author

A STAT1/ETC/GBP1 axis represents a potential therapeutic target for noncommunicable granulomatous skin disease.

Science advances·2026
Same author

Cardiolipin preserves T<sub>reg</sub> metabolic fitness and immune homeostasis in the gut.

Nature metabolism·2026
Same author

FAS-controlled T cells drive lymphoproliferation through glycolysis without effector differentiation.

Journal of human immunity·2026
Same author

MitoSafe hypothesis: safeguarding mitochondrial morphology and innate immunity.

Trends in cell biology·2026
Same author

IL-33 promotes transcriptional and metabolic adaptations of tissue-resident Th2 cells.

Journal of immunology (Baltimore, Md. : 1950)·2026
Same journal

Daily briefing: 'Cyborg' cockroaches breathe underwater with printed suit.

Nature·2026
Same journal

China boosts prestigious grants for young scientists - will it ease competition?

Nature·2026
Same journal

Incoming US science academy chief vows to 'double down' on research.

Nature·2026
Same journal

Author Correction: Synthesis of enantioenriched atropisomers by biocatalytic deracemization.

Nature·2026
Same journal

Electrodeposited self-assembled molecules for perovskite photovoltaics.

Nature·2026
Same journal

Neutrino's nursery found: the 'Shadow Blaster'.

Nature·2026
See all related articles

Related Experiment Video

Updated: Aug 27, 2025

Isolation and Th17 Differentiation of Na&#239;ve CD4 T Lymphocytes
12:59

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes

Published on: September 26, 2013

34.7K

An LKB1-mitochondria axis controls TH17 effector function.

Francesc Baixauli1, Klara Piletic1, Daniel J Puleston1

  • 1Max Planck Institute for Immunobiology and Epigenetics, Freiburg, Germany.

Nature
|September 28, 2022
PubMed
Summary
This summary is machine-generated.

Mitochondrial fusion protein OPA1 is crucial for T helper 17 (TH17) cell function. Liver-associated kinase B1 (LKB1) links mitochondrial changes to TH17 cell cytokine expression.

More Related Videos

Author Spotlight: Achieving High-Purity In Vitro Differentiation of Th17 Cells Using Cytokine Concentration Modulation
07:46

Author Spotlight: Achieving High-Purity In Vitro Differentiation of Th17 Cells Using Cytokine Concentration Modulation

Published on: October 25, 2024

3.3K
Retroviral CRISPR/Cas9-Mediated Gene Targeting for the Study of Th17 Differentiation in Vitro
12:08

Retroviral CRISPR/Cas9-Mediated Gene Targeting for the Study of Th17 Differentiation in Vitro

Published on: November 15, 2024

604

Related Experiment Videos

Last Updated: Aug 27, 2025

Isolation and Th17 Differentiation of Na&#239;ve CD4 T Lymphocytes
12:59

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes

Published on: September 26, 2013

34.7K
Author Spotlight: Achieving High-Purity In Vitro Differentiation of Th17 Cells Using Cytokine Concentration Modulation
07:46

Author Spotlight: Achieving High-Purity In Vitro Differentiation of Th17 Cells Using Cytokine Concentration Modulation

Published on: October 25, 2024

3.3K
Retroviral CRISPR/Cas9-Mediated Gene Targeting for the Study of Th17 Differentiation in Vitro
12:08

Retroviral CRISPR/Cas9-Mediated Gene Targeting for the Study of Th17 Differentiation in Vitro

Published on: November 15, 2024

604

Area of Science:

  • Immunology
  • Cell Biology
  • Metabolic Biology

Background:

  • CD4+ T cell differentiation requires metabolic reprogramming.
  • Mitochondrial membrane dynamics are essential for cellular processes, but their role in T cell differentiation is unclear.

Purpose of the Study:

  • To investigate the role of mitochondrial membrane dynamics, specifically OPA1, in CD4+ T cell differentiation.
  • To elucidate the mechanisms by which mitochondrial function influences TH17 cell effector programs.

Main Methods:

  • T cell-specific deletion of OPA1 in mice.
  • Multi-omics analysis (metabolomics, transcriptomics).
  • Biochemical assays to assess mitochondrial respiration, TCA cycle flux, and metabolite levels.

Main Results:

  • TH17 cells exhibit fused mitochondria with tight cristae, unlike other CD4+ T cell subsets.
  • OPA1 deletion in TH17 cells impairs TCA cycle metabolism, leading to altered metabolite profiles and epigenetic changes.
  • LKB1 acts as a sensor, linking mitochondrial membrane status to IL-17 expression in TH17 cells.

Conclusions:

  • OPA1 is a key regulator of TH17 cell metabolism and function.
  • LKB1 integrates mitochondrial cues to control TH17 cell effector differentiation.
  • Targeting OPA1 or LKB1 may offer therapeutic strategies for TH17 cell-mediated diseases.