Background:
Rheumatoid arthritis (RA) is a chronic systemic inflammatory disease and inhibiting the resultant cytokine production provides a treatment paradigm to control autoimmunity and chronic inflammation.With all the excitement and hype related to these newer “biologic agents” commonly used, disease modifying drugs (DMARDs) such as methotrexate, leflunomide, cyclosporine, hydroxychloroquine have fallen out of focus. The reality is that biologics (alone) are generally no better than methotrexate alone. In these study we invest the effects of anti-arthritis drugs on the resultant cytokine.
Methods:
The 2B4.11 murine T cell hybridoma recognizing cytochrome c as the antigen was co-cultured with the antigen presenting B cell hybridoma line LK35.2 (I-Ek bearing), pigeon cytochrome c and anti-arthritic drugs. After 16 hr incubation the supernatant was removed and cytokines assayed using commercially available kits.
Results:
Anti-arthritic drugs inhibited pro-inflammatory cytokines IL-2, IL-6, IFN-g, GM-CSF to varying amounts. Inhibition was cytokine specific. Leflunomide, salazopyrine, prednisone and indomethacin as well as blocking a Th1 response also stimulated the production of anti-inflammatory cytokine IL-10.
Conclusions:
Anti-arthritic medications can induce a direct inhibition of pro-inflammatory cytokines as well as inciting a Th2 response that could lead to better disease outcomes.