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

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

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 (Humira),...
Tumor Immunotherapy01:27

Tumor Immunotherapy

Immunotherapy is a treatment that boosts or manipulates the immune system to fight diseases, including cancer. For instance, by stimulating an immune response through vaccinations against viruses that cause cancers, like hepatitis B virus and human papillomavirus, these diseases can be prevented. Nonetheless, some cancer cells can avoid the immune system due to their rapid mutation and division. The immune response to many cancers involves three phases: elimination, equilibrium, and escape.
Cytotoxic Edema: Pathophysiology01:21

Cytotoxic Edema: Pathophysiology

Cytotoxic edema is a form of cerebral edema characterized by intracellular swelling of neurons, astrocytes, and other glial cells. It develops when the mechanisms responsible for maintaining ionic gradients across the cell membrane become impaired. Under normal physiological conditions, the sodium–potassium ATPase actively transports sodium ions out of the cell and potassium ions into the cell, preserving osmotic balance and enabling electrical signaling. This pump requires a continuous supply...
T Cell Types and Functions01:24

T Cell Types and Functions

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...
Therapeutic Drug Monitoring: Affecting Factors01:29

Therapeutic Drug Monitoring: Affecting Factors

Therapeutic Drug Monitoring (TDM) is the clinical practice of measuring specific drug levels in a patient's blood or body tissues to manage and optimize therapy. TDM is crucial for drugs with narrow therapeutic windows, like warfarin and phenytoin, where incorrect doses can lead to treatment failure or severe side effects. This monitoring ensures the dosage administered is within a safe and effective range. The factors affecting therapeutic drug monitoring include:Patient-Specific Factors:a.
NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

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 heterodimer of NF-κB...

You might also read

Related Articles

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

Sort by
Same author

Synthesis and characterization of soquelitinib a selective ITK inhibitor that modulates tumor immunity.

npj drug discovery·2026
Same author

Long-Term Tolerability and Safety of AAV5-Id3 Gene Therapy to Eyes.

Translational vision science & technology·2026
Same author

Soquelitinib inhibition of IL-2-inducible T cell kinase ameliorates lung damage in murine models of systemic sclerosis.

Arthritis research & therapy·2025
Same author

Complexities in the Terminology Used for Describing, Diagnosing, and Classifying Retinal Vasculitis: A Scoping Review from the International Uveitis Study Group (IUSG) Retinal Vasculitis Study (ReViSe)-Report 6.

Ocular immunology and inflammation·2025
Same author

Microbiome signatures and their role in uveitis: Pathogenesis, diagnostics, and therapeutic perspectives.

Progress in retinal and eye research·2025
Same author

Clinical trials and quasi-experimental studies in the treatment of noninfectious retinal vasculitis: A systematic review from the International Uveitis Study Group (IUSG) Retinal Vasculitis Study (ReViSe) - Report 4.

Survey of ophthalmology·2025

Related Experiment Video

Updated: Jul 11, 2026

Primed Mycobacterial Uveitis (PMU) as a Model for Post-Infectious Uveitis
10:33

Primed Mycobacterial Uveitis (PMU) as a Model for Post-Infectious Uveitis

Published on: December 17, 2021

Do tumor necrosis factor inhibitors cause uveitis? A registry-based study.

Lyndell L Lim1, Frederick W Fraunfelder, James T Rosenbaum

  • 1Centre for Eye Research Australia, University of Melbourne, East Melbourne, Victoria, Australia. limllp@unimelb.edu.au

Arthritis and Rheumatism
|October 2, 2007
PubMed
Summary

Tumor necrosis factor (TNF) inhibitors like etanercept may cause uveitis, unlike other TNF inhibitors. If uveitis develops during etanercept treatment, switching to infliximab may be a safer option.

More Related Videos

Experimental Autoimmune Uveitis: An Intraocular Inflammatory Mouse Model
07:40

Experimental Autoimmune Uveitis: An Intraocular Inflammatory Mouse Model

Published on: January 12, 2022

Related Experiment Videos

Last Updated: Jul 11, 2026

Primed Mycobacterial Uveitis (PMU) as a Model for Post-Infectious Uveitis
10:33

Primed Mycobacterial Uveitis (PMU) as a Model for Post-Infectious Uveitis

Published on: December 17, 2021

Experimental Autoimmune Uveitis: An Intraocular Inflammatory Mouse Model
07:40

Experimental Autoimmune Uveitis: An Intraocular Inflammatory Mouse Model

Published on: January 12, 2022

Area of Science:

  • Ophthalmology
  • Rheumatology
  • Pharmacology

Background:

  • Population studies suggest TNF inhibitors prevent uveitis in ankylosing spondylitis.
  • Anecdotal reports link etanercept to uveitis, contrasting with general findings.

Purpose of the Study:

  • To assess reported uveitis cases linked to TNF inhibitors using drug event databases.
  • To compare the risk of uveitis associated with etanercept, infliximab, and adalimumab.

Main Methods:

  • Reviewed US uveitis cases reported to two databases before January 1, 2006.
  • Analyzed cases associated with etanercept, infliximab, and adalimumab therapies.

Main Results:

  • Etanercept showed a higher association with uveitis compared to infliximab and adalimumab, even after adjusting for patient numbers.
  • After excluding cases potentially related to underlying disease, etanercept remained significantly associated with more uveitis cases.

Conclusions:

  • Etanercept therapy is linked to more uveitis cases than infliximab or adalimumab, suggesting a drug-specific effect.
  • The findings support that this is not a class effect of TNF inhibitors but specific to certain drugs.
  • Switching to infliximab may be considered if uveitis develops during etanercept treatment.