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Statins do not influence clinical response and B cell depletion after rituximab treatment in rheumatoid arthritis
  1. Sudipto Das1,
  2. Meritxell Fernandez Matilla1,
  3. Shouvik Dass1,
  4. Maya H Buch1,
  5. Andrew C Rawstron2,
  6. Edward M Vital1,
  7. Paul Emery1
  1. 1Division of Rheumatic & Musculoskeletal Disease, NIHR Leeds Biomedical Research Unit, Leeds Institute of Molecular Medicine, Leeds Teaching Hospitals NHS Trust and University of Leeds, Leeds, UK
  2. 2Haematological Malignancy Diagnostic Service, Leeds Teaching Hospitals NHS Trust, Leeds, UK
  1. Correspondence to Professor Paul Emery, Division of Rheumatic & Musculoskeletal Disease, NIHR Leeds Biomedical Research Unit, Leeds Institute of Molecular Medicine, Academic Unit of Musculoskeletal Disease, Leeds Teaching Hospitals NHS Trust and University of Leeds, Chapel Allerton Hospital, Leeds LS7 4SA, UK; p.emery{at}leeds.ac.uk

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B cell depletion by rituximab requires cross linking of CD20, which induces redistribution of CD20 to lipid rafts. This redistribution is correlated with efficiency of complement-dependent cytotoxicity (CDC) and antibody-dependent cell-mediated cytotoxicity (ADCC) in previous studies. The integrity of the lipid rafts may also be important in induction of apoptosis. In vitro, statins interfere with the formation of cholesterol-rich micro domains within the plasma membrane- the lipid rafts, which impairs lymphoma cell killing by ADCC and CDC by rituximab.1 We previously demonstrated that pre- and post-treatment numbers of plasmablasts were associated with clinical response to rituximab.2 Statins were recently reported to inhibit rituximab's clinical efficacy in rheumatoid arthritis (RA).3 We therefore tested for an association of statin use and both …

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