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

2.2K
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...
2.2K
NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

9.8K
The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...
9.8K
Inflammatory Response01:28

Inflammatory Response

16.1K
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,...
16.1K
Regulation of the Unfolded Protein Response01:31

Regulation of the Unfolded Protein Response

2.9K
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...
2.9K
Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF01:24

Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF

506
Tumor Necrosis Factor (TNF), a proinflammatory cytokine, contributes significantly to the inflammation seen in Crohn's disease. It exists as soluble TNF and membrane-bound TNF, with actions mediated through TNF receptors (TNFR). TNFR activation leads to the release of proinflammatory cytokines, T-cell activation, collagen production, and leukocyte migration, all contributing to inflammation in Crohn's disease. Anti-TNF monoclonal antibodies, namely infliximab (Remicade), adalimumab...
506
Antimicrobial Proteins01:23

Antimicrobial Proteins

13.0K
Antimicrobial proteins are important components of the immune system. They aid the body in combating pathogens by either killing them directly or hindering their replication processes. Four main types of antimicrobial substances are interferons, the complement system, iron-binding proteins, and antimicrobial proteins.
Interferons
Interferons (IFNs) are proteins produced by lymphocytes, macrophages, and fibroblasts infected with viruses. While IFNs cannot prevent viruses from entering and...
13.0K

You might also read

Related Articles

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

Sort by
Same author

No-known-vector flaviviruses exhibit diverse replication and virulence phenotypes in mice.

bioRxiv : the preprint server for biology·2026
Same author

Constitutive interferon epsilon expression shapes antiviral epithelial states in the female reproductive tract and intestine.

mBio·2026
Same author

Interferon lambda signaling to maternal dendritic cells protects against congenital Zika virus infection.

bioRxiv : the preprint server for biology·2026
Same author

Cellular and immune adaptations at the maternal-fetal interface in bats.

Cell reports·2025
Same author

Constitutive Interferon Epsilon Expression Shapes Antiviral Epithelial States in the Female Reproductive Tract and Intestine.

bioRxiv : the preprint server for biology·2025
Same author

Cellular and Immune Adaptations at the Maternal-Fetal Interface in Bats.

bioRxiv : the preprint server for biology·2025

Related Experiment Video

Updated: Jan 19, 2026

Native Polyacrylamide Gel Electrophoresis Immunoblot Analysis of Endogenous IRF5 Dimerization
08:57

Native Polyacrylamide Gel Electrophoresis Immunoblot Analysis of Endogenous IRF5 Dimerization

Published on: October 6, 2019

10.7K

Why Is IFN-λ Less Inflammatory? One IRF Decides.

Rebecca L Casazza1, Helen M Lazear1

  • 1Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.

Immunity
|September 19, 2019
PubMed
Summary

Type I and type III interferons activate antiviral programs, but type I is more inflammatory. A new study shows the transcription factor IRF1 selectively drives this inflammation via chemokine expression.

Area of Science:

  • Immunology
  • Molecular Biology
  • Virology

Background:

  • Type I and type III interferons (IFNs) induce comparable antiviral gene expression programs.
  • However, type I IFNs elicit a more pronounced inflammatory response compared to type III IFNs.

Purpose of the Study:

  • To investigate the molecular mechanisms underlying the differential inflammatory potential of type I IFN signaling.
  • To identify key transcription factors mediating the inflammatory aspects of type I IFN responses.

Main Methods:

  • Analysis of gene expression profiles following type I and type III IFN stimulation.
  • Investigation of transcription factor induction and activity, specifically IRF1.
  • Assessment of chemokine expression downstream of IFN signaling pathways.

More Related Videos

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

13.8K
An ELISA Based Binding and Competition Method to Rapidly Determine Ligand-receptor Interactions
08:40

An ELISA Based Binding and Competition Method to Rapidly Determine Ligand-receptor Interactions

Published on: March 14, 2016

20.1K

Related Experiment Videos

Last Updated: Jan 19, 2026

Native Polyacrylamide Gel Electrophoresis Immunoblot Analysis of Endogenous IRF5 Dimerization
08:57

Native Polyacrylamide Gel Electrophoresis Immunoblot Analysis of Endogenous IRF5 Dimerization

Published on: October 6, 2019

10.7K
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

13.8K
An ELISA Based Binding and Competition Method to Rapidly Determine Ligand-receptor Interactions
08:40

An ELISA Based Binding and Competition Method to Rapidly Determine Ligand-receptor Interactions

Published on: March 14, 2016

20.1K

Main Results:

  • Type I IFN signaling selectively induces the transcription factor Interferon Regulatory Factor 1 (IRF1).
  • IRF1 activation is critical for the expression of proinflammatory chemokines in response to type I IFNs.
  • This IRF1-mediated pathway contributes to the heightened inflammatory nature of type I IFN responses.

Conclusions:

  • The transcription factor IRF1 plays a key role in mediating the proinflammatory effects of type I IFNs.
  • Selective IRF1 induction distinguishes the inflammatory output of type I IFN signaling from type III IFN signaling.
  • Targeting the IRF1 pathway could offer strategies to modulate IFN-induced inflammation.