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

Inhibitors of Viral Protein Synthesis01:30

Inhibitors of Viral Protein Synthesis

Protein synthesis is indispensable for viral replication, as viruses lack the cellular machinery required for this process and must hijack the host's translational apparatus. In response, host cells deploy a critical innate immune defense involving interferons, specialized cytokines that play a central role in inhibiting viral propagation.Upon viral detection, infected cells release interferons that bind to receptors on adjacent uninfected cells, activating the JAK-STAT signaling pathway and...
Autoimmune Disorders01:29

Autoimmune Disorders

Autoimmune diseases are a group of disorders in which the body's immune system mistakenly attacks its own cells, tissues, and organs. This results from an overactive immune response against substances and tissues normally present in the body. Let's delve into the concept and mechanism of autoimmune diseases from an immune system point of view, explore different causes and examples of such diseases, and discuss potential solutions.
Concept and Mechanism of Autoimmune Diseases
The immune system...
Immunodeficiency Diseases01:25

Immunodeficiency Diseases

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 disorders...
Immune Response Against Viral Pathogens01:29

Immune Response Against Viral Pathogens

The immune system's response to viral infections is a complex and coordinated process involving natural killer (NK) cells, T cell-mediated responses, and antibody-mediated responses.
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...
Inhibitors Of Virion Release01:25

Inhibitors Of Virion Release

Viral replication and dissemination rely on efficient mechanisms for host cell entry, genome replication, assembly, and release. Influenza viruses, such as types A and B, are negative-sense single-stranded RNA viruses with a segmented genome, that depend on two critical surface glycoproteins to carry out these processes: hemagglutinin (HA) and neuraminidase (NA). HA initiates infection by binding to sialic acid residues on the surface of host epithelial cells, facilitating receptor-mediated...
Experimental RNAi02:15

Experimental RNAi

RNA interference (RNAi) is a cellular mechanism that inhibits gene expression by suppressing its transcription or activating the RNA degradation process. The mechanism was discovered by Andrew Fire and Craig Mello in 1998 in plants. Today, it is observed in almost all eukaryotes, including protozoa, flies, nematodes, insects, parasites, and mammals. This precise cellular mechanism of gene silencing has been developed into a technique that provides an efficient way to identify and determine the...

You might also read

Related Articles

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

Sort by
Same author

Longitudinal Assessment of Cardiac Native T1 in Transfusion-Dependent Thalassemia.

Reviews in cardiovascular medicine·2026
Same author

Liver Diffusion Weighted MRI: Effect of Iron Overload on Apparent Diffusion Coefficient.

NMR in biomedicine·2026
Same author

Immunotherapy for Fertility in Autoimmune Premature Ovarian Insufficiency.

NEJM evidence·2026
Same author

Pancreatic Iron Overload Is Associated With Early QTc Prolongation Before Myocardial Iron Deposition in Transfusion-Dependent Thalassemia.

European journal of haematology·2026
Same author

Independent prognostic value of left ventricular stroke volume index in patients with takotsubo syndrome: insights from the EVOLUTION registry.

Heart (British Cardiac Society)·2026
Same author

Addison's disease in Italy: mortality and survival by etiology.

Journal of endocrinological investigation·2026
Same journal

Tagraxofusp, Azacitidine, and Venetoclax in Blastic Plasmacytoid Dendritic Cell Neoplasm.

Blood·2026
Same journal

Concurrent administration of BCMA and GPRC5D chimeric antigen receptor (CAR) T cells in advanced multiple myeloma.

Blood·2026
Same journal

Single Cell Analysis of the Tumor Microenvironment Landscape Across the Disease Spectrum of Multiple Myeloma.

Blood·2026
Same journal

Decentralized Clinical Trials in Hematology: the Promise and the Peril.

Blood·2026
Same journal

How I Treat Chemotherapy-Induced Thrombocytopenia with Thrombopoietin Receptor Agonists.

Blood·2026
Same journal

The Chaos of Choice in Large B-cell Lymphoma: A Call to Harmonize First-line Trial Design.

Blood·2026
See all related articles

Related Experiment Video

Updated: Jul 3, 2026

High-throughput Quantitative Real-time RT-PCR Assay for Determining Expression Profiles of Types I and III Interferon Subtypes
10:00

High-throughput Quantitative Real-time RT-PCR Assay for Determining Expression Profiles of Types I and III Interferon Subtypes

Published on: March 24, 2015

Interferon autoantibodies associated with AIRE deficiency decrease the expression of IFN-stimulated genes.

Kai Kisand1, Maire Link, Anette S B Wolff

  • 1Institute of General and Molecular Pathology, University of Tartu, Tartu, Estonia.

Blood
|July 9, 2008
PubMed
Summary
This summary is machine-generated.

Autoimmune polyendocrinopathy candidiasis ectodermal dystrophy (APECED) patients have autoantibodies against type I interferons (IFNs). These autoantibodies block IFN-alpha, impairing immune responses and leading to dysregulated IFN activity in this autoimmune disease.

More Related Videos

Development and Validation of an Ultrasensitive Single Molecule Array Digital Enzyme-linked Immunosorbent Assay for Human Interferon-α
08:26

Development and Validation of an Ultrasensitive Single Molecule Array Digital Enzyme-linked Immunosorbent Assay for Human Interferon-α

Published on: June 14, 2018

Related Experiment Videos

Last Updated: Jul 3, 2026

High-throughput Quantitative Real-time RT-PCR Assay for Determining Expression Profiles of Types I and III Interferon Subtypes
10:00

High-throughput Quantitative Real-time RT-PCR Assay for Determining Expression Profiles of Types I and III Interferon Subtypes

Published on: March 24, 2015

Development and Validation of an Ultrasensitive Single Molecule Array Digital Enzyme-linked Immunosorbent Assay for Human Interferon-α
08:26

Development and Validation of an Ultrasensitive Single Molecule Array Digital Enzyme-linked Immunosorbent Assay for Human Interferon-α

Published on: June 14, 2018

Area of Science:

  • Immunology
  • Endocrinology
  • Genetics

Background:

  • Autoimmune polyendocrinopathy candidiasis ectodermal dystrophy (APECED) is caused by AIRE gene mutations affecting thymic T-cell selection.
  • High titers of neutralizing autoantibodies to type I interferons (IFNs), but not type II IFNs, are present in nearly all APECED patients.

Purpose of the Study:

  • To investigate the impact of autoantibodies against type I IFNs on gene expression in APECED patients.
  • To explore the role of IFN dysregulation in the pathogenesis of APECED.

Main Methods:

  • Genome-wide expression array and real-time RT-PCR assays were used to analyze gene expression.
  • Blood cells from APECED patients were cultured to assess the effect of autoantibodies and maturation on IFN-stimulated gene expression.

Main Results:

  • Antibodies against IFN-alpha significantly down-regulated interferon-stimulated gene expression in APECED patient cells by blocking endogenous IFNs.
  • This down-regulation diminished as cells matured in culture without autoantibodies.
  • A rare APECED patient with autoantibodies to IFN-omega (but not IFN-alpha) showed increased expression of interferon-stimulated genes.
  • Unexpectedly increased serum CXCL10 levels were observed in APECED patients.

Conclusions:

  • The breakdown of tolerance to IFNs in AIRE deficiency is linked to impaired thymic responses to IFNs.
  • APECED represents another autoimmune condition characterized by dysregulated interferon activity.