Article Text

PDF
Nucleosome accumulation and reduction of C-reactive protein are associated with the generation of anti-nuclear antibodies in patients with rheumatoid arthritis treated with adalimumab, but not with etanercept
  1. R Priori1,
  2. C Alessandri1,
  3. L Magrini1,
  4. E A M Cassarà1,
  5. F Ceccarelli1,
  6. M Modesti1,
  7. C Croia1,
  8. M Bombardieri2,
  9. G Valesini1
  1. 1
    Dipartimento di Clinica e Terapia Medica, Reumatologia, “Sapienza” Università di Roma, Roma, Italy
  2. 2
    William Harvey Research Institute, Centre for Experimental Medicine and Rheumatology, London, UK
  1. Correspondence to Professor G Valesini, Dipartimento di Clinica e Terapia Medica, Reumatologia, “Sapienza” Università di Roma, Viale del Policlinico 155, 00161 Roma, Italy; guido.valesini{at}uniroma1.it

Statistics from Altmetric.com

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 …

View Full Text

Request permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.