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 Experiment Videos

Why does chronic inflammatory joint disease persist?

Christopher D Buckley1

  • 1Department of Rheumatology, City Hospital NHS Trust, University of Birmingham.

Clinical Medicine (London, England)
|August 27, 2003
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

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

Sort by
Same author

The embryonic origins of site-specific arthritis.

Nature immunology·2026
Same author

Targeting fibroblasts in immune mediated inflammatory diseases: a cellular basis for cure?

Rheumatology (Oxford, England)·2026
Same author

Tissue resident memory T cells populate the human uveal tract.

Scientific reports·2026
Same author

CD64 binding potential does not translate into enhanced therapeutic efficacy for anti-IL-23 antibodies under physiologically relevant conditions.

Molecular medicine (Cambridge, Mass.)·2026
Same author

Cellular and molecular landscapes of human tendons across the lifespan revealed by spatial and single-cell transcriptomics.

Cell reports·2026
Same author

Tissue Damage in Rheumatoid Arthritis Is Genetically Linked to Low Peptidylglycine Alpha-Amidating Monooxygenase Activity in Synovial Fibroblasts.

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

Premature ventricular complexes.

Clinical medicine (London, England)·2026
Same journal

Heart failure with preserved ejection fraction (HFpEF): diagnosis and management for the general physician.

Clinical medicine (London, England)·2026
Same journal

Trends and Widening Inequities in Cardiovascular-Kidney-Metabolic Involvement in Cardiovascular Mortality: A National Spatiotemporal Analysis, 2014-2023.

Clinical medicine (London, England)·2026
Same journal

Educating current and future healthcare professionals on evidence-based sustainable medicine.

Clinical medicine (London, England)·2026
Same journal

UK Foundation Programme training needs a national minimum standard for advanced life support.

Clinical medicine (London, England)·2026
Same journal

Prognostic value of left atrial diameter in chronic kidney disease: The KNOW-CKD study.

Clinical medicine (London, England)·2026
See all related articles

In rheumatoid arthritis (RA), fibroblasts contribute to chronic inflammation by altering immune cell behavior, promoting their survival and retention within the joint. This drives the persistence of inflammation, distinguishing RA from acute, resolving inflammatory responses.

Area of Science:

  • Immunology
  • Rheumatology
  • Cell Biology

Background:

  • Inflammation is a normal host defense mechanism against tissue damage.
  • Most inflammatory episodes resolve spontaneously without lasting effects.
  • In rheumatoid arthritis (RA), inflammation persists, leading to joint tissue damage.

Purpose of the Study:

  • To investigate the drivers of persistent inflammation in RA.
  • To determine the role of infiltrating leukocytes and stromal cells, particularly fibroblasts, in maintaining chronic inflammation.
  • To understand how the synovial microenvironment contributes to RA pathogenesis.

Main Methods:

  • The study focuses on the functional roles of fibroblasts within the RA joint.
  • Analysis of cytokine and chemokine production by synovial fibroblasts.

Related Experiment Videos

  • Assessment of fibroblast-leukocyte interactions and their impact on immune cell behavior.

    • Main Results:

    • Fibroblasts significantly shape the disordered synovial microenvironment in RA.
    • Fibroblasts produce cytokines and chemokines that promote inappropriate survival and retention of leukocytes.
    • These actions of fibroblasts contribute to the accumulation of lymphocytes in the joint.

    Conclusions:

    • Fibroblasts play a critical role in the transition from acute to chronic arthritis.
    • Fibroblast-mediated alterations in the microenvironment are key to persistent inflammation in RA.
    • Targeting fibroblast activity may offer a therapeutic strategy for managing chronic inflammatory diseases like RA.