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

47
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...
47
Type I Diabetes II: Pathophysiology01:26

Type I Diabetes II: Pathophysiology

6
Type 1 diabetes mellitus arises from an immune-mediated destruction of pancreatic β-cells, resulting in an absolute deficiency of insulin. This process develops in genetically susceptible individuals when autoimmunity, environmental exposures, and immunologic dysregulation converge to trigger a targeted attack on the insulin-producing cells of the pancreas. The β-cells are located within the islets of Langerhans and are essential for regulating blood glucose by facilitating cellular...
6
Type I Diabetes I: Introduction01:12

Type I Diabetes I: Introduction

6
Type 1 diabetes mellitus is a chronic metabolic disorder characterized by an absolute deficiency of insulin resulting from the autoimmune destruction of pancreatic β-cells. Although it can occur at any age, it is most commonly diagnosed in childhood, adolescence, or early adulthood. The loss of insulin production impairs cellular glucose uptake, resulting in persistent hyperglycemia and necessitating lifelong insulin therapy.Autoimmune Destruction of β-CellsThe hallmark of type 1...
6
T Cell Types and Functions01:24

T Cell Types and Functions

3.5K
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...
3.5K
Types of Intermediate Filaments01:31

Types of Intermediate Filaments

5.3K
The intermediate filaments are an essential component of the cytoskeleton. Presently six types of intermediate filament have been identified. Type I and II are acidic and basic keratin proteins. Type III is of mesodermal origin and comprises four proteins: vimentin, desmin, glial fibrillary acidic protein (GFAP), and peripherin. Vimentin is commonly found in mesenchymal cells, desmin in muscle cells, GFAP in astrocytes, while peripherin is found in peripheral nervous system neurons (PNS). Type...
5.3K
Regulation of the Unfolded Protein Response01:31

Regulation of the Unfolded Protein Response

3.3K
Inositol-requiring kinase one or IRE1 is the most conserved eukaryotic unfolded protein response (UPR) receptor. It is a type I transmembrane protein kinase receptor with a distinctive site-specific RNase activity. As the binding mechanics of the misfolded proteins with the N-terminal domain of IRE-1 are unclear, three binding models — direct, indirect, and allosteric -- are proposed for receptor activation. Nevertheless, it is known that once a misfolded protein associates with IRE1, it...
3.3K

You might also read

Related Articles

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

Sort by
Same author

ADAR1 loss-of-function variants altering RNA editing define a new interferon-dependent psoriasis subtype.

The Journal of experimental medicine·2026
Same author

Early brain-penetrant immunotherapy reverses interferon signature and improves motor outcome in a case of ADAR1-related Aicardi-Goutières syndrome.

Clinical & translational immunology·2026
Same author

Nuclear STING compromises replication fidelity.

Nature reviews. Immunology·2026
Same author

Familial lupus associated with a <i>P2RY8</i> variant: Navigating the boundary between monogenic disease and genetic susceptibility to lupus.

Journal of human immunity·2026
Same author

A transcriptomic microglia taxonomy across mouse and human pathologies.

Nature immunology·2026
Same author

<i>TLR7</i> mutations leading to enhanced TLR7 signaling in humans.

Journal of human immunity·2026

Related Experiment Video

Updated: Apr 20, 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

13.9K

Type I interferonopathies: mendelian type I interferon up-regulation.

Yanick J Crow1

  • 1INSERM UMR 1163, Laboratory of Neurogenetics and Neuroinflammation, Paris, France; Paris Descartes - Sorbonne Paris Cité University, Institute Imagine, Paris, France; Manchester Centre for Genomic Medicine, Institute of Human Development Faculty of Medical and Human Sciences, Manchester Academic Health Sciences Centre, University of Manchester, UK.

Current Opinion in Immunology
|December 3, 2014
PubMed
Summary

Type I interferonopathies are a newly identified group of Mendelian disorders. Research is progressing to better understand these inborn errors of immunity.

More Related Videos

Development and Validation of an Ultrasensitive Single Molecule Array Digital Enzyme-linked Immunosorbent Assay for Human Interferon-&#945;
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

12.7K
A High Resolution Method to Monitor Phosphorylation-dependent Activation of IRF3
11:44

A High Resolution Method to Monitor Phosphorylation-dependent Activation of IRF3

Published on: January 24, 2016

12.6K

Related Experiment Videos

Last Updated: Apr 20, 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

13.9K
Development and Validation of an Ultrasensitive Single Molecule Array Digital Enzyme-linked Immunosorbent Assay for Human Interferon-&#945;
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

12.7K
A High Resolution Method to Monitor Phosphorylation-dependent Activation of IRF3
11:44

A High Resolution Method to Monitor Phosphorylation-dependent Activation of IRF3

Published on: January 24, 2016

12.6K

Area of Science:

  • Immunology
  • Genetics
  • Infectious Diseases

Background:

  • Mendelian disorders are genetic conditions inherited from parents.
  • Type I interferons are crucial signaling proteins in the immune system.
  • Recent research suggests a link between certain Mendelian disorders and increased type I interferon activity.

Purpose of the Study:

  • To discuss the progress in defining and understanding type I interferonopathies.
  • To highlight this novel category of inborn errors of immunity.

Main Methods:

  • Review of recent scientific literature.
  • Analysis of clinical and genetic data related to type I interferonopathies.

Main Results:

  • The concept of type I interferonopathies is gaining traction in the scientific community.
  • Progress is being made in characterizing the genetic basis and clinical manifestations of these disorders.

Conclusions:

  • Type I interferonopathies represent a significant new area of research in inborn errors of immunity.
  • Further investigation is needed to fully elucidate the mechanisms and therapeutic strategies for these conditions.