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Cytokines in rheumatoid arthritis
Margriet J B M Vervoordeldonk1, Paul P Tak
1Division of Clinical Immunology and Rheumatology, Department of Medicine, Academic Medical Center, University of Amsterdam, PO box 22660, 1100 DD Amsterdam, The Netherlands. M.J.Vervoordeldonk@amc.uva.nl
Current Rheumatology Reports
|May 16, 2002
Summary
Rheumatoid arthritis involves chronic inflammation driven by cytokines. Research highlights the roles of interleukin-18 and T helper 1 cell cytokines in joint destruction, while T helper 2 cells may offer protection.
Area of Science:
- Immunology
- Rheumatology
Background:
- Rheumatoid arthritis (RA) is a chronic inflammatory disease affecting synovial joints.
- Cytokines, particularly monokines from macrophages, are key in RA pathogenesis.
- Pro-inflammatory cytokines like IL-1 and TNF-alpha are established contributors to RA.
Purpose of the Study:
- To review the role of cytokines in rheumatoid arthritis.
- To highlight the significance of IL-18 in inflammatory joint diseases.
- To discuss the balance between pro-inflammatory (Th1) and potentially protective (Th2) cytokines in RA.
Main Methods:
- Review of recent research on cytokine expression and regulation in RA.
- Analysis of the abundance of monokines versus lymphokines in rheumatoid synovial tissue.
- Examination of the contribution of T cell-derived cytokines (Th1 and Th2) to RA.
Main Results:
- Pro-inflammatory cytokines, including IL-1, TNF-alpha, and IL-18, are crucial in RA development and progression.
- Monokines are abundant in RA synovial tissue, while lymphokines are less prevalent.
- Th1 cell-derived cytokines contribute to joint inflammation and destruction, whereas Th2 cell products may be protective.
Conclusions:
- Cytokine dysregulation, particularly involving IL-18 and Th1 responses, drives RA pathogenesis.
- A compensatory anti-inflammatory response exists in the RA synovial membrane.
- Targeting specific cytokine pathways, considering the balance between Th1 and Th2 responses, may offer therapeutic strategies for RA.