Abstract
Anti-TNFs have become a benchmark in the treatment of numerous autoimmune diseases such as rheumatoid arthritis, Crohn’s disease, and psoriasis. However, TNF blockade as a therapy has its limitations. Besides an increased susceptibility to infections, 0.2-1% of patients develop anti-TNF induced lupus erythematosus (ATIL). Moreover, anti-TNFs are associated with increased frequencies of anti-drug antibodies (ADA). We have previously shown that TNF inhibition shifts the equilibrium of TNF and type I interferons towards an excessive type I interferon response.
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