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During the last decade, three tumour necrosis factor (TNF)α antagonists have been approved for the treatment of moderate to severe rheumatoid arthritis (RA).1 These new drugs, while extremely powerful, can induce puzzling biological phenomena such as the production of autoantibodies whose extent seems to vary accordingly to the drug used.2,3
A dysregulation of apoptosis with exposition of nuclear antigens and consequent rapid (within hours) accumulation of nucleosomes has been evoked to explain autoantibody occurrence in patients treated with infliximab.4 In addition (or in alternative) to an increased release of nuclear antigens, a defect in clearance mechanisms can play a role in the generation of autoantibodies.5
We studied autoantibody profiles (anti-nuclear antibody (ANA), anti-double stranded …
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