Journal
CLINICAL IMMUNOLOGY
Volume 203, Issue -, Pages 28-36Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.clim.2019.03.009
Keywords
Rheumatoid arthritis; Antirheumatic treatment; Endogenous DNA damage; DNA repair; Chromatin organization; Oxidative stress
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Funding
- IKY [2018-050-0502-13136]
- ELKE [0974]
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We investigated the DNA damage response and repair network in 18 patients with active rheumatoid arthritis and tested the hypothesis that treatment influences this network. A 3-fold increase of endogenous DNA damage (single- and double-strand breaks) was detected in patient-derived peripheral blood mononuclear cells than controls (alkaline comet assay; mean +/- SD Olive Tail Moment of 11.8 +/- 7.3 versus 4.3 +/- 2.2, p < .001). Patients exhibited significantly higher formation of DNA damage (oxidative stress and a basic sites), deficient global genome repair and more condensed chromatin structure than controls. Twelve weeks following treatment, chromatin structure loosened, global genome repair capacity was restored, oxidative stress and a basic sites decreased and levels of endogenous DNA damage reached control values in all 8 patients examined. We conclude that deregulated chromatin organization, deficient DNA repair capacity and augmented formation of DNA damage, which are reversible after treatment, contribute to the accumulation of endogenous DNA damage in rheumatoid arthritis.
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