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Several autoimmune diseases, most notably systemic lupus erythematosus (SLE), show an overexpression of type I interferon (IFN)-inducible genes, termed the IFN signature.1 The IFN signature is associated with endothelial progenitor cells (EPC) dysfunction in SLE2 and the recent report by Grenn et al3 provides evidence for this link in antiphospholipid syndrome (APS) as well.
The authors show that patients with primary APS (PAPS) have a reduced number of circulating EPC that differentiate into endothelial cell like cells. This is supported by a similar reduction in EPC differentiation when EPC from healthy controls (HC) are cultured with serum from patients with PAPS. Whereas depletion of antiphospholipid antibodies (aPL) has no effect, blockade of the receptor for type I IFN restores EPC differentiation. Hence, targeting type I IFN might mitigate vascular disease in patients with APS by restoring EPC differentiation. In support of this assumption, the authors demonstrate the presence of an IFN signature in peripheral blood mononuclear cells (PBMC) of patients with PAPS.
Previous hints in the literature further confirm the presence of an IFN signature in PBMC of patients with PAPS.4 ,5 Interestingly, a microarray study on isolated monocytes of patients with SLE, SLE+APS and PAPS reported the presence of an IFN signature only in monocytes of patients with SLE and SLE+APS, not in PAPS.6 Monocytes are considered key players in the pathogenesis of APS4 among others due to an overexpression of tissue factor (TF), the main initiator of humoral coagulation, while shifts in monocyte subsets are linked to vascular disease in rheumatic diseases.7 ,8
Here we report the …
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