Deregulated DNA damage response network in Behcet's disease.

Autor: Vlachogiannis NI; Joint Rheumatology Program, National and Kapodistrian University of Athens Medical School, Athens, Greece. Electronic address: nvlachog@med.uoa.gr., Ntouros PA; Joint Rheumatology Program, National and Kapodistrian University of Athens Medical School, Athens, Greece., Pappa M; Joint Rheumatology Program, National and Kapodistrian University of Athens Medical School, Athens, Greece., Verrou KM; Joint Rheumatology Program, National and Kapodistrian University of Athens Medical School, Athens, Greece; Center of New Biotechnologies & Precision Medicine, National and Kapodistrian University of Athens Medical School, Athens, Greece., Arida A; Joint Rheumatology Program, National and Kapodistrian University of Athens Medical School, Athens, Greece., Souliotis VL; Joint Rheumatology Program, National and Kapodistrian University of Athens Medical School, Athens, Greece; Institute of Chemical Biology, National Hellenic Research Foundation, Athens, Greece., Sfikakis PP; Joint Rheumatology Program, National and Kapodistrian University of Athens Medical School, Athens, Greece; Center of New Biotechnologies & Precision Medicine, National and Kapodistrian University of Athens Medical School, Athens, Greece. Electronic address: psfikakis@med.uoa.gr.
Jazyk: angličtina
Zdroj: Clinical immunology (Orlando, Fla.) [Clin Immunol] 2023 Jan; Vol. 246, pp. 109189. Date of Electronic Publication: 2022 Nov 16.
DOI: 10.1016/j.clim.2022.109189
Abstrakt: 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.
Competing Interests: Declaration of Competing Interest There are no competing interests for any author.
(Copyright © 2022 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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