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

678
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...
678
Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents01:29

Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents

621
Crohn's disease is an inflammatory bowel disorder marked by chronic inflammation of the GI tract. Various treatment strategies for Crohn's disease are employed, such as immunomodulatory agents, glucocorticoids, and biologics or anti-TNF therapy. Azathioprine (Imuran), a commonly used immunomodulatory drug for Crohn's disease, is converted in the body to mercaptopurine, which inhibits purine biosynthesis and cell proliferation. Both are utilized in severe cases of Inflammatory Bowel...
621
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

13.5K
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...
13.5K
T Cell Types and Functions01:24

T Cell Types and Functions

3.0K
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...
3.0K
Inflammatory Bowel Disease II: Crohn's Disease01:30

Inflammatory Bowel Disease II: Crohn's Disease

1.4K
Introduction
Inflammatory bowel disease, commonly known as IBD, refers to a collection of disorders that lead to persistent inflammation of the gastrointestinal tract. The two types of IBD are ulcerative colitis, which impacts the colon, and Crohn's disease, which can involve any part of the gastrointestinal segment.
Crohn's disease
Crohn's disease is a chronic, systemic inflammatory bowel disease (IBD) that predominantly affects the gastrointestinal tract. It is marked by...
1.4K
Inflammatory Response01:28

Inflammatory Response

17.9K
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,...
17.9K

You might also read

Related Articles

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

Sort by
Same author

Are Glucocorticoids Associated With Worse Survival Among Patients With Rheumatoid Arthritis and Lung Cancer Treated With Immune Checkpoint Inhibitors?

Arthritis & rheumatology (Hoboken, N.J.)·2025
Same author

Arthroplasty Joint Histology and Surgical Outcomes in Patients on Immune Checkpoint Inhibitors: A Single-Center Case Series.

The Journal of rheumatology·2025
Same author

Use of Apremilast for the Treatment of Immune Checkpoint Inhibitor Psoriasis and Psoriatic Arthritis.

Arthritis care & research·2025
Same author

Survival in Immune Checkpoint Inhibitor-Treated Patients With Rheumatoid Arthritis and Non-Small Cell Lung Cancer: An Observational Cohort Study.

Arthritis care & research·2025
Same author

The Current and Future of Biomarkers of Immune Related Adverse Events.

Immunology and allergy clinics of North America·2025
Same author

Barriers to Total Joint Arthroplasty: A Comparison of High-Poverty and Low-Poverty Communities.

Arthritis care & research·2024
Same journal

Same Family, Different Stories: Distinct Peripheral Immune Signatures in Axial Spondyloarthritis and Psoriatic Arthritis.

Arthritis & rheumatology (Hoboken, N.J.)·2026
Same journal

ACR Treatment Guidelines and Expert Opinion: The Continuum of Knowledge Guiding Clinical Decision-Making.

Arthritis & rheumatology (Hoboken, N.J.)·2026
Same journal

DNA (cytosine-5)-methyltransferase 3A (Dnmt3a) mutations limit normal and autoreactive CD4+ T follicular helper responses and attenuate T cell-driven joint inflammation.

Arthritis & rheumatology (Hoboken, N.J.)·2026
Same journal

Treatment of Patients with CPPD Disease: Where Do We Begin and Where Are We Going?

Arthritis & rheumatology (Hoboken, N.J.)·2026
Same journal

Efficacy and Safety of Nanoencapsulated Sirolimus plus Pegadricase: Results from the Randomized, Placebo-Controlled Phase 3 Trials.

Arthritis & rheumatology (Hoboken, N.J.)·2026
Same journal

Fibroblast Mitochondrial Ca2+ Overload Drives Skin Fibrosis via mtDNA Leakage and cGAS-STING Activation in Systemic Sclerosis.

Arthritis & rheumatology (Hoboken, N.J.)·2026
See all related articles

Related Experiment Video

Updated: Mar 10, 2026

Adoptive Immunotherapy of iNKT Cells in Glucose-6-Phosphate Isomerase G6PI-Induced RA Mice
08:43

Adoptive Immunotherapy of iNKT Cells in Glucose-6-Phosphate Isomerase G6PI-Induced RA Mice

Published on: January 31, 2020

7.4K

Immune Checkpoint Inhibitor-Associated Inflammatory Arthritis.

Sang T Kim1, Anne R Bass2

  • 1Department of Rheumatology, Allergy & Immunology, Yale University, New Haven, Connecticut.

Arthritis & Rheumatology (Hoboken, N.J.)
|March 9, 2026
PubMed
Summary
This summary is machine-generated.

Immune checkpoint inhibitors (ICI) can cause inflammatory arthritis (ICI-IA), characterized by specific T cell and macrophage activity. Understanding ICI-IA offers insights into other inflammatory arthritis mechanisms.

More Related Videos

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

1.3K
A Cryo-pulverization Protocol for Processing Mouse Paws to Evaluate Molecular Pathways of Tissue Inflammation in a Collagen Induced Arthritis Model
11:03

A Cryo-pulverization Protocol for Processing Mouse Paws to Evaluate Molecular Pathways of Tissue Inflammation in a Collagen Induced Arthritis Model

Published on: October 30, 2019

9.2K

Related Experiment Videos

Last Updated: Mar 10, 2026

Adoptive Immunotherapy of iNKT Cells in Glucose-6-Phosphate Isomerase G6PI-Induced RA Mice
08:43

Adoptive Immunotherapy of iNKT Cells in Glucose-6-Phosphate Isomerase G6PI-Induced RA Mice

Published on: January 31, 2020

7.4K
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

1.3K
A Cryo-pulverization Protocol for Processing Mouse Paws to Evaluate Molecular Pathways of Tissue Inflammation in a Collagen Induced Arthritis Model
11:03

A Cryo-pulverization Protocol for Processing Mouse Paws to Evaluate Molecular Pathways of Tissue Inflammation in a Collagen Induced Arthritis Model

Published on: October 30, 2019

9.2K

Area of Science:

  • Immunology
  • Oncology
  • Rheumatology

Background:

  • Immune checkpoint inhibitors (ICIs) like PD-1 and CTLA-4 blockers revolutionized cancer therapy.
  • However, ICIs can cause autoimmune side effects, notably immune checkpoint inhibitor-associated inflammatory arthritis (ICI-IA) in ~6% of patients.
  • ICI-IA often mimics rheumatoid arthritis but is typically seronegative, with imaging revealing joint inflammation even without swelling.

Purpose of the Study:

  • To review the current understanding of the cellular and molecular mechanisms of ICI-IA.
  • To explore the role of specific immune cells and signaling pathways in ICI-IA pathogenesis.
  • To identify potential research avenues for ICI-IA and other inflammatory arthritides.

Main Methods:

  • Review of existing literature on ICI-IA.
  • Analysis of cellular and molecular characteristics of ICI-IA synovium.
  • Examination of immune cell populations (T cells, macrophages, Tregs) and signaling axes (CXCL10-CXCR3, CCR1-CCL3/5).

Main Results:

  • ICI-IA synovium shows clonal expansion of CD38hiCD127-CD8+ T cells and IL-1βhi macrophages.
  • Communication occurs along CXCL10-CXCR3 and CCR1-CCL3/5 pathways.
  • Naïve CD4+ T cell activation and impaired regulatory T cells (Tregs) synergistically amplify inflammation, particularly with combination ICI therapy.

Conclusions:

  • ICI-IA pathogenesis involves specific T cell and macrophage activation patterns and signaling pathways.
  • Understanding ICI-IA provides valuable insights into the broader mechanisms of inflammatory arthritis.
  • Further research into ICI-IA could inform the development of targeted therapies for both ICI-induced autoimmunity and other forms of arthritis.