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. 2020 Oct 2;11:582401. doi: 10.3389/fimmu.2020.582401

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Copyright © 2020 Vlachogiannis, Pappa, Ntouros, Nezos, Mavragani, Souliotis and Sfikakis

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Deregulated DNA repair mechanisms in SSc. (A) Line-graphs showing the kinetics of γH2AX formation and removal 0–24 h after treatment of freshly isolated PBMCs from HC (n=9) and SSc patients (n=9) with melphalan. (B) Confocal microscopy images showing γH2AX staining at different time points after the ex vivo treatment of PBMCs from a representative HC and an SSc patient with melphalan. Upper images, immunofluorescence antigen staining; middle, cell nuclei labeled with DAPI; bottom, merged. (C) Tukey boxplots representing DNA DSB accumulation (γH2Ax immunofluorescence) 24 h after treatment with melphalan. (D) Line graphs showing levels of single- and double-strand DNA breaks (Olive tail moment) as assessed by alkaline comet assay in PBMCs of HC (n=24) and SSc patients (n=22) at baseline and 1, 2, and 6 h after ex vivo UVC irradiation of freshly isolated PBMCs with 5J/m². (E) Tukey boxplots representing DNA SSB and DSB accumulation (alkaline comet assay) 6 h after treatment of PBMCs with 5J/m² UVC. *P<0.05 compared to controls.