ABSTRACT
Introduction: Rheumatoid arthritis (RA) is a chronic, deforming arthritis that can lead to disabilities and poor quality of life. Cytokines are protein mediators of inflammation and are produced as a result of the activation of various cellular reactions. They are the final mediators and/or regulators of the inflammatory process. Materials and Methods: The sera from 64 RA patients were assayed for both Th-1 and Th-2 related cytokines and soluble TNF-α receptors (IFN-γ, TGF-β, TNF-α, IL-1β, IL-2, IL-4, IL-6, IL-8, IL-10, IL-12, IL-18, sTNF-R1 and sTNFR2) using ELISA. Results: The pro-inflammatory cytokines (IL-1, IL-6, IL-8, IL-18 and TNFα) were significantly elevated in RA patients, while TGF-β, an immunomodulatory cytokine, was elevated in control individuals. When the RA patients were categorised as active or inactive based on DAS scores, similar cytokines profiles were observed in both RA sub-groups. However, assays of sTNF-R1 and sTNFR-2 were noted to be significantly elevated in inactive RA patients when compared to active patients. Conclusion: Our findings indicate that local production of cytokine inhibitors is capable of diminishing disease activity and cytokine activity.
Rheumatoid arthritis (RA) is a chronic autoimmune disease characterised by severe joint deformities due to bony erosions and tendon damage. The chronic inflammatory process is mediated through a complex cytokine network. The clinical expressions and outcome of the disease can vary among different ethnic groups, possibly depending upon the differential expressions of MHC and cytokine genes. Cytokines are protein messengers that convey information between and within cells via specific cell surface receptor molecules. The release of specific cytokines into the systemic circulation has been observed in a variety of inflammatory disease including RA. Their concentration levels usually reflect disease severity and prognosis. However, since most cytokines are expressed transiently and can be induced or inhibited by other cytokines, it has been suggested that a “cytokine network” may exist in which cytokines regulate each other.1,2 Cytokines are also divided into pro-inflammatory cytokines (TNF-α, IFN-γ, IL-1, IL-2, IL-6, IL-8, IL-12 and IL-18) and anti-inflammatory cytokines (IL-4, IL-10, TGF-β). In RA, the balance between pro-inflammatory and anti-inflammatory cytokines determines the degree and extent of inflammation, and thus can lead to different clinical effects. Anti-inflammatory cytokines or cytokine antagonists counteract the effects of pro-inflammatory cytokines and therefore the relative concentration of a cytokine to its inhibitor or antagonist will determine its final effect.
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