Immunological intervention reveals reciprocal roles for tumor necrosis factor-alpha and interleukin-10 in rheumatoid arthritis and systemic lupus erythematosus.
In RA (and in collagen-induced arthritis in DBA/l mice) experimental evidence has convincingly demonstrated the therapeutic benefit of anti-TNF-α antibodies, whereas anti-TNF-α also induces lupus-associated DNA antibodies in a minority of presumably genetically susceptible individuals, and accelerates SLE nephritis in NZB/W mice whose disease is suppressed by anti-IL-10. Conversely, TNF-α replacement protects NZB/W F1 mice from developing SLE, as does anti-IL-10 therapy, by inducing TNF-α. Li...Expand abstract
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