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

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...
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
Inflammatory Bowel Disease III: Crohn's Disease01:25

Inflammatory Bowel Disease III: Crohn's Disease

Crohn’s disease is a chronic, relapsing form of inflammatory bowel disease characterized by segmental, transmural inflammation that can affect any part of the gastrointestinal tract. Its pathogenesis arises from a combination of genetic susceptibility, environmental exposures, epithelial barrier dysfunction, and immune dysregulation. Together, these factors lead to an exaggerated immune response against components of the gut microbiome.Genetic and Environmental InfluencesMultiple genetic...
Inflammatory Bowel Disease II: Ulcerative Colitis01:20

Inflammatory Bowel Disease II: Ulcerative Colitis

Ulcerative colitis is a chronic inflammatory disorder of the colon characterized by continuous mucosal inflammation that typically begins in the rectum and extends proximally in a uniform pattern. Its pathogenesis involves a complex interplay of genetic predisposition, immune dysregulation, and environmental influences. These factors converge to impair the colon’s epithelial defenses and promote an exaggerated inflammatory response against luminal contents.Breakdown of the Mucosal BarrierA...
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),...
Inflammatory Response01:28

Inflammatory Response

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,...

You might also read

Related Articles

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

Sort by
Same author

Proteome-wide autoantibody screening and holistic autoantigenomic analysis unveil COVID-19 signature of autoantibody landscape.

BMC immunology·2026
Same author

Glucocorticoid sparing in rheumatoid arthritis patients treated with Janus kinase inhibitors: insights from the Japanese patient registry.

Scientific reports·2026
Same author

Successful Reintroduction of Golimumab in a Patient With Rheumatoid Arthritis and Prolonged Epstein-Barr Virus Reactivation With Persistent Anti-Viral Capsid Antigen IgM Antibodies: A Case Report.

Cureus·2026
Same author

Transcriptome analysis unveils Th1 cell cycle signature as a distinctive feature of mixed connective tissue disease.

Arthritis research & therapy·2025
Same author

Identification of Potential Therapeutic Agents for Type I Interferonopathy Using iPSC-Based Disease Modeling.

Journal of clinical immunology·2025
Same author

Anti-U1-RNP antibody positivity is associated with elevated interferon-stimulated gene expression scores in systemic lupus erythematosus irrespective of disease activity: a transcriptome analysis in Japanese patients.

Modern rheumatology·2025

Related Experiment Video

Updated: Jul 10, 2026

An Adoptive Transfer Model of Rheumatoid Arthritis in Mice
07:37

An Adoptive Transfer Model of Rheumatoid Arthritis in Mice

Published on: June 6, 2025

[Rheumatoid arthritis and interleukin-32].

Hirofumi Shoda1, Keishi Fujio, Kazuhiko Yamamoto

  • 1Department of Allergy and Rheumatology, Graduate School of Medicine, the University of Tokyo.

Nihon Rinsho Men'Eki Gakkai Kaishi = Japanese Journal of Clinical Immunology
|November 7, 2007
PubMed
Summary

Interleukin-32 (IL-32) significantly contributes to rheumatoid arthritis pathogenesis by promoting inflammatory cytokine cascades. Elevated IL-32 levels in patients correlate with disease severity, highlighting its role in arthritis development.

Related Experiment Videos

Last Updated: Jul 10, 2026

An Adoptive Transfer Model of Rheumatoid Arthritis in Mice
07:37

An Adoptive Transfer Model of Rheumatoid Arthritis in Mice

Published on: June 6, 2025

Area of Science:

  • Immunology
  • Rheumatology

Context:

  • Rheumatoid arthritis (RA) pathogenesis involves complex inflammatory cytokine networks.
  • Interleukin-32 (IL-32) is a recently identified human cytokine implicated in inflammation.

Purpose:

  • To investigate the role of IL-32 in the pathogenesis of rheumatoid arthritis.
  • To explore the expression and function of IL-32 in RA synovial tissues and experimental models.

Summary:

  • IL-32 induces key inflammatory cytokines like TNF-alpha, IL-1beta, and IL-6 from immune cells.
  • IL-32 expression is elevated in RA synovial tissues and correlates with disease severity.
  • Experimental models show that IL-32 promotes joint inflammation and exacerbates arthritis.

Impact:

  • IL-32 is a critical mediator in rheumatoid arthritis.
  • Targeting IL-32 may offer a novel therapeutic strategy for RA treatment.