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Correspondence response
Response to: ‘Monocyte type I interferon signature in antiphospholipid syndrome is related to pro-inflammatory monocyte subsets, hydroxychloroquine and statin use’ by van den Hoogen et al
  1. Srilakshmi Yalavarthi,
  2. Robert C Grenn,
  3. Jason S Knight
  1. Division of Rheumatology, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA
  1. Correspondence to Dr Jason S Knight, Division of Rheumatology, Department of Internal Medicine, University of Michigan, 5520A MSRB1, 1150 W Medical Center Drive, SPC 5680, Ann Arbor, MI 48109-5680, USA; jsknight{at}

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Primary antiphospholipid syndrome (APS) is an autoimmune disorder of unknown cause, characterised by not only thrombotic events and pregnancy morbidity but also accelerated atherosclerosis. We reviewed with great interest the letter by van den Hoogen et al,1 which comments on our recent paper.2 In our study, we discovered a defect in endothelial progenitor function in patients with primary APS—such defects have been described as predecessors to atherosclerosis. We subsequently revealed a type I interferon (IFN) signature in peripheral blood mononuclear cells of the same patients. Importantly, inhibition of the type I IFN receptor restored normal differentiation of endothelial progenitors into endothelial cells in vitro. Further, we detected the IFN signature not only in our local primary APS cohort but also in a cohort of patients from Mexico.

van den Hoogen et al1 have now detected a type I IFN signature in a third cohort of patients with primary APS, this one recruited in the Netherlands. Going further, they reanalysed …

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