Abstract
Dear Editor, We read with great interest the article by Skaug et al. [1], recently published in Rheumatology, in which the authors focus on the functional consequences of the DNASE1L3 R206C variant, by determining its impact on the digestion of circulating genomic DNA (gDNA) in SSc patients and healthy controls. DNASE1L3, also known as DNAase γ, an endonuclease expressed predominantly by dendritic cells and macrophages, is secreted into the circulation, where it has a unique ability to digest gDNA in apoptosis-derived membrane vesicles (AdMVs). Aiming to elucidate the mechanism by which this variant increases SSc susceptibility, the authors made a new and valuable contribution and clearly confirmed in their paper that circulating gDNA is a physiological DNASE1L3 substrate. Moreover, they showed that its digestion is reduced in SSc patients carrying the R206C (rs35677470) variant. SSc is a chronic, multisystem autoimmune disease, clinically characterized by progressive skin and internal organ fibrosis, producing various clinical manifestations including inflammation, autoimmunity and vasculopathy, and exhibiting one of the highest mortality rates among rheumatic diseases [2].
Published Version
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