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

Immunodeficiency Diseases01:25

Immunodeficiency Diseases

2.7K
Immunodeficiency disorders are conditions in which the immune system's ability to fight infectious disease and cancer is compromised or entirely absent. The immune system comprises a complex network of cells, tissues, and organs that work together to protect the body from potentially harmful invaders. When this system is deficient or not functioning properly, it leaves the body susceptible to infections, diseases, or other complications.
There are three main causes of immunodeficiency...
2.7K
T Cell Types and Functions01:24

T Cell Types and Functions

2.9K
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...
2.9K
T Cell Activation and Clonal Selection01:22

T Cell Activation and Clonal Selection

16.7K
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...
16.7K
Cytotoxic T Cells-mediated Immune Response01:27

Cytotoxic T Cells-mediated Immune Response

7.7K
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...
7.7K
Cystic Fibrosis: Pathogenesis01:23

Cystic Fibrosis: Pathogenesis

954
Cystic fibrosis (CF), an autosomal recessive disorder, significantly affects the function of exocrine glands. This genetically inherited disease is characterized by the production of thick and sticky mucus, which can severely affect various organs and systems in the body.
CF is primarily caused by a genetic mutation in a chromosome 7 gene coding for the cystic fibrosis transmembrane conductance regulator (CFTR) protein. The most common gene mutation leading to CF is the ΔF508 mutation,...
954
B Cell Activation and Differentiation01:24

B Cell Activation and Differentiation

17.4K
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...
17.4K

You might also read

Related Articles

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

Sort by
Same author

Fusion gene heterogeneity and kinase enrichment in high-grade serous carcinomas.

Neoplasia (New York, N.Y.)·2026
Same author

Clinical Practice Guideline for the diagnosis of Granulomatous-Lymphocytic Interstitial Lung Disease (GLILD) in patients with Common Variable Immunodeficiency Disorders (CVID) - an ERS Clinical Research Collaboration.

The European respiratory journal·2026
Same author

Arginine Deprivation of ASS1-Deficient Cancers Drives Mistranslation and Shared Neoepitope Production.

Cancer research·2026
Same author

Vaccination of immunosuppressed patients.

Tidsskrift for den Norske laegeforening : tidsskrift for praktisk medicin, ny raekke·2026
Same author

Distinct Proteomic and Transcriptomic Profiles in T-cells and Monocytes in Patients with Common Variable Immunodeficiency: an Exploratory Study.

Journal of clinical immunology·2026
Same author

High-Throughput Phenotypic Screen to Identify FoxP3 Regulators in Primary T Cells.

ACS chemical biology·2026

Related Experiment Video

Updated: Mar 3, 2026

Author Spotlight: Elucidating the Pathways of TFH Cell Differentiation in Acute LCMV Challenges
05:03

Author Spotlight: Elucidating the Pathways of TFH Cell Differentiation in Acute LCMV Challenges

Published on: April 26, 2024

1.3K

Defective IL-4 signaling in T cells defines severe common variable immunodeficiency.

Eli Taraldsrud1, Børre Fevang2, Silje F Jørgensen2

  • 1Department of Cancer Immunology, Institute for Cancer Research, Oslo University Hospital, Radiumhospitalet, Oslo, Norway; K.G. Jebsen Center for Cancer Immunotherapy and K.G. Jebsen Inflammation Research Center, Institute of Clinical Medicine, University of Oslo, Oslo, Norway; Research Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway.

Journal of Autoimmunity
|May 7, 2017
PubMed
Summary

Common variable immunodeficiency (CVID) patients with severe complications show impaired IL-4 signaling in T cells. This defect, linked to lower IL-4Rα and JAK1, contributes to inflammation and autoimmunity in CVID.

Keywords:
AutoimmunityCVIDHypogammaglobulinemiaIL-4 signalingIL-4RαPhospho-flow cytometryT cellTh1

More Related Videos

Phenotypic and Functional Analysis of Activated Regulatory T Cells Isolated from Chronic Lymphocytic Choriomeningitis Virus-infected Mice
07:17

Phenotypic and Functional Analysis of Activated Regulatory T Cells Isolated from Chronic Lymphocytic Choriomeningitis Virus-infected Mice

Published on: June 22, 2016

10.4K
Isolating Human Peripheral Blood Mononuclear Cells and CD4+ T cells from Sézary Syndrome Patients for Transcriptomic Profiling
09:08

Isolating Human Peripheral Blood Mononuclear Cells and CD4+ T cells from Sézary Syndrome Patients for Transcriptomic Profiling

Published on: October 14, 2021

6.4K

Related Experiment Videos

Last Updated: Mar 3, 2026

Author Spotlight: Elucidating the Pathways of TFH Cell Differentiation in Acute LCMV Challenges
05:03

Author Spotlight: Elucidating the Pathways of TFH Cell Differentiation in Acute LCMV Challenges

Published on: April 26, 2024

1.3K
Phenotypic and Functional Analysis of Activated Regulatory T Cells Isolated from Chronic Lymphocytic Choriomeningitis Virus-infected Mice
07:17

Phenotypic and Functional Analysis of Activated Regulatory T Cells Isolated from Chronic Lymphocytic Choriomeningitis Virus-infected Mice

Published on: June 22, 2016

10.4K
Isolating Human Peripheral Blood Mononuclear Cells and CD4+ T cells from Sézary Syndrome Patients for Transcriptomic Profiling
09:08

Isolating Human Peripheral Blood Mononuclear Cells and CD4+ T cells from Sézary Syndrome Patients for Transcriptomic Profiling

Published on: October 14, 2021

6.4K

Area of Science:

  • Immunology
  • Cellular Biology
  • Clinical Medicine

Background:

  • Common variable immunodeficiency (CVID) is characterized by hypogammaglobulinemia and B-cell dysfunction, leading to heterogeneous clinical presentations.
  • Severe non-infectious complications, including autoimmunity and granulomatous disease, significantly impact CVID patient morbidity.
  • T-cell abnormalities are implicated in CVID pathogenesis, but specific functional T-cell characteristics linked to clinical subtypes remain unclear.

Purpose of the Study:

  • To investigate functional T-cell signaling pathways in response to common gamma-chain cytokines in CVID patients.
  • To correlate T-cell signaling defects with specific clinical subtypes of CVID, particularly severe non-infectious complications.
  • To elucidate the molecular mechanisms underlying potential T-cell dysfunction in CVID.

Main Methods:

  • Analysis of peripheral blood T cells from 29 CVID patients and 19 healthy donors.
  • Assessment of cytokine-induced phosphorylation of STAT3, STAT5, and STAT6 in response to IL-2, IL-4, IL-7, and IL-21.
  • Evaluation of T-helper (Th)1/Th2 polarization and expression of IL-4 receptor and downstream signaling molecules.

Main Results:

  • A subgroup of 7 CVID patients exhibited impaired IL-4-induced p-STAT6 signaling in naive and memory CD4 and CD8 T cells.
  • This IL-4 signaling defect correlated with the highest burden of severe non-infectious complications and persisted over time.
  • Lower mRNA levels of IL-4Rα and JAK1 were observed in these patients, suggesting a molecular basis for the impaired IL-4 signaling and a Th1 bias.

Conclusions:

  • Identified a distinct subgroup of CVID patients with defective IL-4 signaling in T cells.
  • This signaling defect is associated with severe clinical manifestations, including inflammation and autoimmunity.
  • The findings highlight the role of IL-4 signaling pathways in CVID pathogenesis and suggest potential therapeutic targets.