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Article ; Online: Augmented oxidative stress, accumulation of DNA damage and impaired DNA repair mechanisms in thrombotic primary antiphospholipid syndrome.

Pappa, Maria / Ntouros, Panagiotis A / Papanikolaou, Christina / Sfikakis, Petros P / Souliotis, Vassilis L / Tektonidou, Maria G

Clinical immunology (Orlando, Fla.)

2023 Volume 254, Page(s) 109693

Abstract: Antiphospholipid syndrome (APS) is a rare autoimmune disorder with complex pathogenesis. Studies have shown that oxidative stress may contribute to APS pathophysiology. In peripheral blood mononuclear cells (PBMCs) from thrombotic Primary APS (thrPAPS) ... ...

Abstract	Antiphospholipid syndrome (APS) is a rare autoimmune disorder with complex pathogenesis. Studies have shown that oxidative stress may contribute to APS pathophysiology. In peripheral blood mononuclear cells (PBMCs) from thrombotic Primary APS (thrPAPS) patients and age/sex-matched healthy controls (HC), as well as a control group of asymptomatic antiphospholipid antibody (aPL) positive individuals without APS (aPL+/non-APS), we examined oxidative stress, abasic (apurinic/apyrimidinic) sites, and DNA damage response (DDR)-associated parameters, including endogenous DNA damage (single- and double-strand breaks) and DNA repair mechanisms, namely nucleotide excision repair (NER) and double-strand breaks repair (DSB/R). We found that thrPAPS patients exhibited significantly higher levels of endogenous DNA damage, increased oxidative stress and abasic sites, as well as lower NER and DSB/R capacities versus HC (all P < 0.001) and versus aPL+/non-APS subjects (all P < 0.05). Our findings demonstrate that oxidative stress and decreased DNA repair mechanisms contribute to the accumulation of endogenous DNA damage in PBMCs from thrPAPS patients and, if further validated, may be exploited as therapeutic targets and potential biomarkers.
MeSH term(s)	Humans ; Antiphospholipid Syndrome ; Leukocytes, Mononuclear ; DNA Repair ; Oxidative Stress ; Thrombosis/etiology ; DNA Damage
Language	English
Publishing date	2023-07-16
Publishing country	United States
Document type	Journal Article
ZDB-ID	1459903-x
ISSN	1521-7035 ; 1521-6616
ISSN (online)	1521-7035
ISSN	1521-6616
DOI	10.1016/j.clim.2023.109693
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Article ; Online: Geriatric Frailty Is Associated With Oxidative Stress, Accumulation, and Defective Repair of DNA Double-Strand Breaks Independently of Age and Comorbidities.

Kravvariti, Evrydiki / Ntouros, Panagiotis A / Vlachogiannis, Nikolaos I / Pappa, Maria / Souliotis, Vassilis L / Sfikakis, Petros P

The journals of gerontology. Series A, Biological sciences and medical sciences

2022 Volume 78, Issue 4, Page(s) 603–610

Abstract: Defects in the DNA damage response and repair (DDR/R) network accumulate during the aging process. Physical frailty, a state of reduced physiological function and decreased resilience to biological stressors, is also exacerbated by aging, but its link ... ...

Abstract	Defects in the DNA damage response and repair (DDR/R) network accumulate during the aging process. Physical frailty, a state of reduced physiological function and decreased resilience to biological stressors, is also exacerbated by aging, but its link with DDR/R aberrations beyond the effect of age and comorbidities is unclear. Fifty-three community-dwelling older adults, aged 65-102 years, who underwent frailty classification according to the Rockwood Clinical Frailty Scale (CFS), and 51 healthy adults younger than 45 years were examined in parallel. The following DDR/R parameters were determined in their peripheral blood mononuclear cells (PBMCs): (a) oxidative stress and abasic (apurinic/apyrimidinic; AP) sites, (b) endogenous DNA damage (alkaline comet assay olive tail moment [OTM] indicative of DNA single-strand breaks [SSBs] and double-strand breaks [DSBs] and γH2AX levels by immunofluorescence [DSBs only]), (c) capacity of the 2 main DNA repair mechanisms (DSB repair and nucleotide excision repair). Older individual-derived PBMCs displayed reduced-to-oxidized glutathione ratios indicative of increased levels of oxidative stress and increased AP sites, as well as increased accumulation of endogenous DNA damage (OTM and γH2AX) and defective DSB-repair capacity, compared with younger controls. These DDR/R aberrations were more pronounced in frail versus nonfrail older adults. Notably, oxidative stress, AP sites, DSBs, and DSB-repair capacity were associated with individual CFS levels after adjusting for chronological age, sex, Charlson Comorbidity Index, and polypharmacy. Geriatric frailty is independently associated with increased DNA damage formation and reduced DSB-R capacity, supporting further research into these measures as potential frailty biomarkers.
MeSH term(s)	Humans ; Aged ; DNA Breaks, Double-Stranded ; Leukocytes, Mononuclear ; Frailty/genetics ; DNA Repair/genetics ; Oxidative Stress/genetics ; DNA Damage ; DNA/genetics ; Comorbidity
Chemical Substances	DNA (9007-49-2)
Language	English
Publishing date	2022-10-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1223643-3
ISSN	1758-535X ; 1079-5006
ISSN (online)	1758-535X
ISSN	1079-5006
DOI	10.1093/gerona/glac214
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Article ; Online: Deregulated DNA damage response network in Behcet's disease.

Vlachogiannis, Nikolaos I / Ntouros, Panagiotis A / Pappa, Maria / Verrou, Kleio-Maria / Arida, Aikaterini / Souliotis, Vassilis L / Sfikakis, Petros P

Clinical immunology (Orlando, Fla.)

2022 Volume 246, Page(s) 109189

Abstract: Behcet's disease (BD) is a chronic, relapsing systemic vasculitis of unknown etiology. Since the DNA repair enzyme NEIL1 has been identified as one of the two genetic risk factors for BD by whole exome study, we examined the potential involvement of the ... ...

Abstract	Behcet's disease (BD) is a chronic, relapsing systemic vasculitis of unknown etiology. Since the DNA repair enzyme NEIL1 has been identified as one of the two genetic risk factors for BD by whole exome study, we examined the potential involvement of the DNA damage response (DDR) network in BD. Peripheral blood mononuclear cells from 26 patients and 26 age-/sex-matched healthy controls were studied. Endogenous DNA damage levels were increased in active BD patients compared to controls or patients in remission. In parallel, BD patients had defective nucleotide excision repair capacity. RNA-sequencing revealed reduced expression of NEIL1 that negatively correlated with DNA damage accumulation. On the other hand, expression of genes involved in senescence and senescence-associated secretory phenotype positively correlated with individual endogenous DNA damage levels. We conclude that deregulated DDR contributes to the proinflammatory environment in BD.
MeSH term(s)	Humans ; Behcet Syndrome/complications ; Leukocytes, Mononuclear ; Case-Control Studies ; DNA Glycosylases
Chemical Substances	NEIL1 protein, human (EC 3.2.2.-) ; DNA Glycosylases (EC 3.2.2.-)
Language	English
Publishing date	2022-11-16
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1459903-x
ISSN	1521-7035 ; 1521-6616
ISSN (online)	1521-7035
ISSN	1521-6616
DOI	10.1016/j.clim.2022.109189
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Article: Microvasculopathy-Related Hemorrhagic Tissue Deposition of Iron May Contribute to Fibrosis in Systemic Sclerosis: Hypothesis-Generating Insights from the Literature and Preliminary Findings.

Sfikakis, Petros P / Vlachogiannis, Nikolaos I / Ntouros, Panagiotis A / Mavrogeni, Sophie / Maris, Thomas G / Karantanas, Apostolos H / Souliotis, Vassilis L

Life (Basel, Switzerland)

2022 Volume 12, Issue 3

Abstract: Microvascular wall abnormalities demonstrated by nailfold capillaroscopy in systemic sclerosis (SSc) may result in microhemorrhagic deposition of erythrocyte-derived iron. Such abnormalities precede fibrosis, which is orchestrated by myofibroblasts. Iron ...

Abstract	Microvascular wall abnormalities demonstrated by nailfold capillaroscopy in systemic sclerosis (SSc) may result in microhemorrhagic deposition of erythrocyte-derived iron. Such abnormalities precede fibrosis, which is orchestrated by myofibroblasts. Iron induces endothelial-to-mesenchymal transition in vitro, which is reversed by reactive oxygen species (ROS) scavengers. The conversion of quiescent fibroblasts into profibrotic myofibroblasts has also been associated with ROS-mediated activation of TGF-β1. Given that iron overload predisposes to ROS formation, we hypothesized that the uptake of erythrocyte-derived iron by resident cells promotes fibrosis. Firstly, we show that iron induces oxidative stress in skin-derived and synovial fibroblasts in vitro, as well as in blood mononuclear cells ex vivo. The biological relevance of increased oxidative stress was confirmed by showing the concomitant induction of DNA damage in these cell types. Similar results were obtained in vivo, following intravenous iron administration. Secondly, using magnetic resonance imaging we show an increased iron deposition in the fingers of a patient with early SSc and nailfold microhemorrhages. While a systematic magnetic resonance study to examine tissue iron levels in SSc, including internal organs, is underway, herein we propose that iron may be a pathogenetic link between microvasculopathy and fibrosis and an additional mechanism responsible for increased oxidative stress in SSc.
Language	English
Publishing date	2022-03-16
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2662250-6
ISSN	2075-1729
ISSN	2075-1729
DOI	10.3390/life12030430
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Article ; Online: Type-I interferon pathway and DNA damage accumulation in peripheral blood of patients with psoriatic arthritis.

Fragoulis, George E / Ntouros, Panagiotis A / Nezos, Adrianos / Vlachogiannis, Nikolaos I / McInnes, Iain B / Tektonidou, Maria G / Skarlis, Charalampos / Souliotis, Vassilis L / Mavragani, Clio P / Sfikakis, Petros P

Frontiers in immunology

2023 Volume 14, Page(s) 1274060

Abstract: Objectives: The abnormal DNA damage response is associated with upregulation of the type-1 interferon (IFN-I) pathway in certain rheumatic diseases. We investigated whether such aberrant mechanisms operate in psoriatic arthritis (PsA).: Methods: DNA ... ...

Abstract	Objectives: The abnormal DNA damage response is associated with upregulation of the type-1 interferon (IFN-I) pathway in certain rheumatic diseases. We investigated whether such aberrant mechanisms operate in psoriatic arthritis (PsA). Methods: DNA damage levels were measured by alkaline comet assay in peripheral blood mononuclear cells from 52 PsA patients and age-sex-matched healthy individuals. RNA expression of Results: In PsA, DNA damage accumulation was increased by almost two-fold compared to healthy individuals (olive tail moment arbitrary units, mean ± SD; 9.42 ± 2.71 Conclusion: DNA damage in PsA correlates with measures of inflammation but is not associated with the IFN-I pathway induction. The unexpected IFN-I downregulation, albeit reminiscent to findings in experimental models of spondyloarthritis, may be implicated in PsA pathogenesis and explained by operation of other cytokines.
MeSH term(s)	Humans ; Arthritis, Psoriatic/pathology ; Interferon Type I/metabolism ; Leukocytes, Mononuclear/metabolism ; Interleukin-6/metabolism ; DNA Damage ; RNA/metabolism
Chemical Substances	Interferon Type I ; Interleukin-6 ; RNA (63231-63-0)
Language	English
Publishing date	2023-12-06
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2023.1274060
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Article ; Online: Effective DNA damage response after acute but not chronic immune challenge: SARS-CoV-2 vaccine versus Systemic Lupus Erythematosus.

Ntouros, Panagiotis A / Vlachogiannis, Nikolaos I / Pappa, Maria / Nezos, Adrianos / Mavragani, Clio P / Tektonidou, Maria G / Souliotis, Vassilis L / Sfikakis, Petros P

Clinical immunology (Orlando, Fla.)

2021 Volume 229, Page(s) 108765

Abstract: Whether and how an acute immune challenge may affect DNA Damage Response (DDR) is unknown. By studying vaccinations against Influenza and SARS-CoV-2 (mRNA-based) we found acute increases of type-I interferon-inducible gene expression, oxidative stress ... ...

Abstract	Whether and how an acute immune challenge may affect DNA Damage Response (DDR) is unknown. By studying vaccinations against Influenza and SARS-CoV-2 (mRNA-based) we found acute increases of type-I interferon-inducible gene expression, oxidative stress and DNA damage accumulation in blood mononuclear cells of 9 healthy controls, coupled with effective anti-SARS-CoV-2 neutralizing antibody production in all. Increased DNA damage after SARS-CoV-2 vaccine, partly due to increased oxidative stress, was transient, whereas the inherent DNA repair capacity was found intact. In contrast, in 26 patients with Systemic Lupus Erythematosus, who served as controls in the context of chronic immune activation, we validated increased DNA damage accumulation, increased type-I interferon-inducible gene expression and induction of oxidative stress, however aberrant DDR was associated with deficiencies in nucleotide excision repair pathways. These results indicate that acute immune challenge can indeed activate DDR pathways, whereas, contrary to chronic immune challenge, successful repair of DNA lesions occurs.
MeSH term(s)	Adolescent ; Adult ; Aged ; Antibodies, Neutralizing/physiology ; COVID-19/pathology ; COVID-19/prevention & control ; COVID-19 Vaccines/immunology ; Case-Control Studies ; DNA Damage ; Female ; Gene Expression Regulation/immunology ; Humans ; Interferon Type I/metabolism ; Lupus Erythematosus, Systemic/immunology ; Male ; Middle Aged ; Oxidative Stress ; SARS-CoV-2/immunology ; Vaccines, Synthetic/immunology ; Young Adult ; mRNA Vaccines
Chemical Substances	Antibodies, Neutralizing ; COVID-19 Vaccines ; Interferon Type I ; Vaccines, Synthetic
Language	English
Publishing date	2021-06-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1459903-x
ISSN	1521-7035 ; 1521-6616
ISSN (online)	1521-7035
ISSN	1521-6616
DOI	10.1016/j.clim.2021.108765
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Article ; Online: DNA Damage Response and Oxidative Stress in Systemic Autoimmunity.

Souliotis, Vassilis L / Vlachogiannis, Nikolaos I / Pappa, Maria / Argyriou, Alexandra / Ntouros, Panagiotis A / Sfikakis, Petros P

International journal of molecular sciences

2019 Volume 21, Issue 1

Abstract: The DNA damage response and repair (DDR/R) network, a sum of hierarchically structured signaling pathways that recognize and repair DNA damage, and the immune response to endogenous and/or exogenous threats, act synergistically to enhance cellular ... ...

Abstract	The DNA damage response and repair (DDR/R) network, a sum of hierarchically structured signaling pathways that recognize and repair DNA damage, and the immune response to endogenous and/or exogenous threats, act synergistically to enhance cellular defense. On the other hand, a deregulated interplay between these systems underlines inflammatory diseases including malignancies and chronic systemic autoimmune diseases, such as systemic lupus erythematosus, systemic sclerosis, and rheumatoid arthritis. Patients with these diseases are characterized by aberrant immune response to self-antigens with widespread production of autoantibodies and multiple-tissue injury, as well as by the presence of increased oxidative stress. Recent data demonstrate accumulation of endogenous DNA damage in peripheral blood mononuclear cells from these patients, which is related to (a) augmented DNA damage formation, at least partly due to the induction of oxidative stress, and (b) epigenetically regulated functional abnormalities of fundamental DNA repair mechanisms. Because endogenous DNA damage accumulation has serious consequences for cellular health, including genomic instability and enhancement of an aberrant immune response, these results can be exploited for understanding pathogenesis and progression of systemic autoimmune diseases, as well as for the development of new treatments.
MeSH term(s)	Animals ; Arthritis, Rheumatoid/genetics ; Arthritis, Rheumatoid/immunology ; Arthritis, Rheumatoid/metabolism ; Autoimmune Diseases/genetics ; Autoimmune Diseases/immunology ; Autoimmune Diseases/metabolism ; Autoimmunity ; DNA Damage ; DNA Repair ; Humans ; Lupus Erythematosus, Systemic/genetics ; Lupus Erythematosus, Systemic/immunology ; Lupus Erythematosus, Systemic/metabolism ; Oxidative Stress ; Scleroderma, Systemic/genetics ; Scleroderma, Systemic/immunology ; Scleroderma, Systemic/metabolism
Language	English
Publishing date	2019-12-20
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms21010055
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Article ; Online: Chronological Age and DNA Damage Accumulation in Blood Mononuclear Cells: A Linear Association in Healthy Humans after 50 Years of Age.

Vlachogiannis, Nikolaos I / Ntouros, Panagiotis A / Pappa, Maria / Kravvariti, Evrydiki / Kostaki, Evangelia Georgia / Fragoulis, Georgios E / Papanikolaou, Christina / Mavroeidi, Dimitra / Bournia, Vasiliki-Kalliopi / Panopoulos, Stylianos / Laskari, Katerina / Arida, Aikaterini / Gorgoulis, Vassilis G / Tektonidou, Maria G / Paraskevis, Dimitrios / Sfikakis, Petros P / Souliotis, Vassilis L

International journal of molecular sciences

2023 Volume 24, Issue 8

Abstract: Aging is characterized by the progressive deregulation of homeostatic mechanisms causing the accumulation of macromolecular damage, including DNA damage, progressive decline in organ function and chronic diseases. Since several features of the aging ... ...

Abstract	Aging is characterized by the progressive deregulation of homeostatic mechanisms causing the accumulation of macromolecular damage, including DNA damage, progressive decline in organ function and chronic diseases. Since several features of the aging phenotype are closely related to defects in the DNA damage response (DDR) network, we have herein investigated the relationship between chronological age and DDR signals in peripheral blood mononuclear cells (PBMCs) from healthy individuals. DDR-associated parameters, including endogenous DNA damage (single-strand breaks and double-strand breaks (DSBs) measured by the alkaline comet assay (Olive Tail Moment (OTM); DSBs-only by γH2AX immunofluorescence staining), DSBs repair capacity, oxidative stress, and apurinic/apyrimidinic sites were evaluated in PBMCs of 243 individuals aged 18-75 years, free of any major comorbidity. While OTM values showed marginal correlation with age until 50 years (r
MeSH term(s)	Male ; Humans ; Female ; Middle Aged ; Leukocytes, Mononuclear/physiology ; Prospective Studies ; DNA Breaks, Double-Stranded ; DNA Damage ; Aging/genetics ; DNA Repair
Language	English
Publishing date	2023-04-12
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms24087148
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Article ; Online: Oxidative stress and endogenous DNA damage in blood mononuclear cells may predict anti-SARS-CoV-2 antibody titers after vaccination in older adults.

Ntouros, Panagiotis A / Kravvariti, Evrydiki / Vlachogiannis, Nikolaos I / Pappa, Maria / Trougakos, Ioannis P / Terpos, Evangelos / Tektonidou, Maria G / Souliotis, Vassilis L / Sfikakis, Petros P

Biochimica et biophysica acta. Molecular basis of disease

2022 Volume 1868, Issue 6, Page(s) 166393

Abstract: Immune senescence in the elderly has been associated with chronic oxidative stress and DNA damage accumulation. Herein we tested the hypothesis that increased endogenous DNA damage and oxidative stress in peripheral blood mononuclear cells of older ... ...

Abstract	Immune senescence in the elderly has been associated with chronic oxidative stress and DNA damage accumulation. Herein we tested the hypothesis that increased endogenous DNA damage and oxidative stress in peripheral blood mononuclear cells of older adults associate with diminished humoral immune response to SARS-CoV-2 vaccination. Increased oxidative stress and DNA double-strand breaks (DSBs) were detected in 9 non-immunocompromised individuals aged 80-96 years compared to 11 adults aged 27-44 years, before, as well as on days 1 and 14 after the first dose, and on day 14 after the second dose of the BNT162B2-mRNA vaccine (all p < 0.05). SARS-CoV-2 vaccination induced a resolvable increase in oxidative stress and DNA damage, but individual DSB-repair efficiency was unaffected by vaccination irrespective of age, confirming vaccination safety. Individual titers of anti-Spike-Receptor Binding Domain (S-RBD)-IgG antibodies, and the neutralizing capacity of circulating anti-SARS-CoV-2 antibodies, measured on day 14 after the second dose in all participants, correlated inversely with the corresponding pre-vaccination endogenous oxidative stress and DSB levels (all p < 0.05). In particular, a strong inverse correlation of individual pre-vaccination DSB levels with both the respective anti-S-RBD-IgG antibodies titers (r = -0.867) and neutralizing capacity of circulating anti-SARS-CoV-2 antibodies (r = -0.983) among the 9 older adults was evident. These findings suggest that humoral responses to SARS-CoV-2 vaccination may be weaker when immune cells are under oxidative and/or genomic stress. Whether such measurements may serve as biomarkers of vaccine efficacy in older adults warrants further studies.
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; BNT162 Vaccine ; COVID-19/prevention & control ; COVID-19 Vaccines/adverse effects ; DNA Damage ; Humans ; Leukocytes, Mononuclear ; Oxidative Stress ; SARS-CoV-2 ; Vaccination ; Vaccines, Synthetic ; mRNA Vaccines
Chemical Substances	COVID-19 Vaccines ; Vaccines, Synthetic ; mRNA Vaccines ; BNT162 Vaccine (N38TVC63NU)
Language	English
Publishing date	2022-03-18
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	60-7
ISSN	1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbadis.2022.166393
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Article ; Online: Association Between DNA Damage Response, Fibrosis and Type I Interferon Signature in Systemic Sclerosis.

Vlachogiannis, Nikolaos I / Pappa, Maria / Ntouros, Panagiotis A / Nezos, Adrianos / Mavragani, Clio P / Souliotis, Vassilis L / Sfikakis, Petros P

Frontiers in immunology

2020 Volume 11, Page(s) 582401

Abstract: Increased endogenous DNA damage and type I interferon pathway activation have been implicated in systemic sclerosis (SSc) pathogenesis. Because experimental evidence suggests an interplay between DNA damage response/repair (DDR/R) and immune response, we ...

Abstract	Increased endogenous DNA damage and type I interferon pathway activation have been implicated in systemic sclerosis (SSc) pathogenesis. Because experimental evidence suggests an interplay between DNA damage response/repair (DDR/R) and immune response, we hypothesized that deregulated DDR/R is associated with a type I interferon signature and/or fibrosis extent in SSc. DNA damage levels, oxidative stress, induction of abasic sites and the efficiency of DNA double-strand break repair (DSB/R) and nucleotide excision repair (NER) were assessed in peripheral blood mononuclear cells (PBMCs) derived from 37 SSc patients and 55 healthy controls; expression of DDR/R-associated genes and type I interferon-induced genes was also quantified. Endogenous DNA damage was significantly higher in untreated diffuse or limited SSc (Olive tail moment; 14.7 ± 7.0 and 9.5 ± 4.1, respectively) as well as in patients under cytotoxic treatment (15.0 ± 5.4) but not in very early onset SSc (5.6 ± 1.2) compared with controls (4.9 ± 2.6). Moreover, patients with pulmonary fibrosis had significantly higher DNA damage levels than those without (12.6 ± 5.8 vs. 8.8 ± 4.8, respectively). SSc patients displayed increased oxidative stress and abasic sites, defective DSB/R but not NER capacity, downregulation of genes involved in DSB/R (MRE11A, PRKDC) and base excision repair (PARP1, XRCC1), and upregulation of apoptosis-related genes (BAX, BBC3). Individual levels of DNA damage in SSc PBMCs correlated significantly with the corresponding mRNA expression of type I interferon-induced genes (IFIT1, IFI44 and MX1,
MeSH term(s)	Adult ; Aged ; Apoptosis/genetics ; Autoantibodies/metabolism ; DNA Damage ; DNA Repair/genetics ; Female ; Fibrosis ; Humans ; Interferon Type I/genetics ; Interferon Type I/metabolism ; Lung/pathology ; Male ; Middle Aged ; Oxidative Stress/genetics ; Scleroderma, Systemic/genetics ; Scleroderma, Systemic/immunology
Chemical Substances	Autoantibodies ; Interferon Type I
Language	English
Publishing date	2020-10-02
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2020.582401
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