Matches in SemOpenAlex for { <https://semopenalex.org/work/W1990975553> ?p ?o ?g. }
- W1990975553 endingPage "562" @default.
- W1990975553 startingPage "554" @default.
- W1990975553 abstract "UVR-induced DNA damage is the major molecular trigger for photoimmunosuppression. The cytokines IL-12 and IL-18, which reduce DNA damage through induction of DNA repair, prevent UVR-induced immunosuppression. IL-12 but not IL-18 can break established UVR-induced immunotolerance through modulation of regulatory T cells (Treg). IL-23 is related to IL-12 by sharing the p40 subunit. Hence, we studied whether (i) IL-23 can reduce UVR-induced DNA damage and thereby prevent UVR-induced immunosuppression and (ii) can suppress the activity of Treg. IL-23 reduced UVR-induced apoptosis of keratinocytes. Injection of IL-23 into UVR-exposed mice diminished the number of apoptotic keratinocytes and the amounts of DNA damage. This was not observed in DNA repair-deficient xeroderma pigmentosum A knock-out mice (Xpa-KO mice), implying that IL-23 reduces DNA damage through induction of DNA repair. Similarly, UVR-mediated suppression of the induction of contact hypersensitivity was prevented on injection of IL-23 in wild-type but not in Xpa-KO mice. However, in contrast to IL-18, IL-23 inhibited the activity of UVR-induced Treg as demonstrated by adoptive transfer experiments. Our data indicate that IL-23, similar to IL-12 and IL-18, can reduce UVR-induced DNA damage and thereby prevent immunosuppression. IL-23 shares with IL-12 the still unique capacity to restore suppressed immune responses because of its effect on Treg. UVR-induced DNA damage is the major molecular trigger for photoimmunosuppression. The cytokines IL-12 and IL-18, which reduce DNA damage through induction of DNA repair, prevent UVR-induced immunosuppression. IL-12 but not IL-18 can break established UVR-induced immunotolerance through modulation of regulatory T cells (Treg). IL-23 is related to IL-12 by sharing the p40 subunit. Hence, we studied whether (i) IL-23 can reduce UVR-induced DNA damage and thereby prevent UVR-induced immunosuppression and (ii) can suppress the activity of Treg. IL-23 reduced UVR-induced apoptosis of keratinocytes. Injection of IL-23 into UVR-exposed mice diminished the number of apoptotic keratinocytes and the amounts of DNA damage. This was not observed in DNA repair-deficient xeroderma pigmentosum A knock-out mice (Xpa-KO mice), implying that IL-23 reduces DNA damage through induction of DNA repair. Similarly, UVR-mediated suppression of the induction of contact hypersensitivity was prevented on injection of IL-23 in wild-type but not in Xpa-KO mice. However, in contrast to IL-18, IL-23 inhibited the activity of UVR-induced Treg as demonstrated by adoptive transfer experiments. Our data indicate that IL-23, similar to IL-12 and IL-18, can reduce UVR-induced DNA damage and thereby prevent immunosuppression. IL-23 shares with IL-12 the still unique capacity to restore suppressed immune responses because of its effect on Treg. contact hypersensitivity; CPD, cyclobutane pyrimidine dimer 2,4-dinitrofluorobenzene nucleotide excision repair T helper 17 cell regulatory T cell UVR-induced Treg wild type xeroderma pigmentosum A knock-out mice" @default.
- W1990975553 created "2016-06-24" @default.
- W1990975553 creator A5010920166 @default.
- W1990975553 creator A5019087013 @default.
- W1990975553 creator A5045696724 @default.
- W1990975553 creator A5057450466 @default.
- W1990975553 creator A5063077790 @default.
- W1990975553 date "2010-02-01" @default.
- W1990975553 modified "2023-10-16" @default.
- W1990975553 title "IL-23 Antagonizes UVR-Induced Immunosuppression through Two Mechanisms: Reduction of UVR-Induced DNA Damage and Inhibition of UVR-Induced Regulatory T Cells" @default.
- W1990975553 cites W1912634928 @default.
- W1990975553 cites W1955806191 @default.
- W1990975553 cites W1966657187 @default.
- W1990975553 cites W1997319936 @default.
- W1990975553 cites W1998267570 @default.
- W1990975553 cites W2002147029 @default.
- W1990975553 cites W2007771316 @default.
- W1990975553 cites W2011398706 @default.
- W1990975553 cites W2015742956 @default.
- W1990975553 cites W2034465933 @default.
- W1990975553 cites W2036805524 @default.
- W1990975553 cites W2050806096 @default.
- W1990975553 cites W2069423064 @default.
- W1990975553 cites W2073037264 @default.
- W1990975553 cites W2093395242 @default.
- W1990975553 cites W2100895591 @default.
- W1990975553 cites W2102505588 @default.
- W1990975553 cites W2107711587 @default.
- W1990975553 cites W2128728003 @default.
- W1990975553 cites W2129806196 @default.
- W1990975553 cites W2131018122 @default.
- W1990975553 cites W2132682137 @default.
- W1990975553 cites W2132810497 @default.
- W1990975553 cites W2133408276 @default.
- W1990975553 cites W2134066780 @default.
- W1990975553 cites W2138413317 @default.
- W1990975553 cites W2144028590 @default.
- W1990975553 cites W2170381128 @default.
- W1990975553 cites W2171849343 @default.
- W1990975553 cites W4205117617 @default.
- W1990975553 doi "https://doi.org/10.1038/jid.2009.274" @default.
- W1990975553 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/19727119" @default.
- W1990975553 hasPublicationYear "2010" @default.
- W1990975553 type Work @default.
- W1990975553 sameAs 1990975553 @default.
- W1990975553 citedByCount "30" @default.
- W1990975553 countsByYear W19909755532012 @default.
- W1990975553 countsByYear W19909755532013 @default.
- W1990975553 countsByYear W19909755532014 @default.
- W1990975553 countsByYear W19909755532015 @default.
- W1990975553 countsByYear W19909755532016 @default.
- W1990975553 countsByYear W19909755532017 @default.
- W1990975553 countsByYear W19909755532018 @default.
- W1990975553 countsByYear W19909755532020 @default.
- W1990975553 countsByYear W19909755532021 @default.
- W1990975553 countsByYear W19909755532022 @default.
- W1990975553 countsByYear W19909755532023 @default.
- W1990975553 crossrefType "journal-article" @default.
- W1990975553 hasAuthorship W1990975553A5010920166 @default.
- W1990975553 hasAuthorship W1990975553A5019087013 @default.
- W1990975553 hasAuthorship W1990975553A5045696724 @default.
- W1990975553 hasAuthorship W1990975553A5057450466 @default.
- W1990975553 hasAuthorship W1990975553A5063077790 @default.
- W1990975553 hasBestOaLocation W19909755531 @default.
- W1990975553 hasConcept C134935766 @default.
- W1990975553 hasConcept C143425029 @default.
- W1990975553 hasConcept C153911025 @default.
- W1990975553 hasConcept C203014093 @default.
- W1990975553 hasConcept C2776090121 @default.
- W1990975553 hasConcept C2778378917 @default.
- W1990975553 hasConcept C2780252810 @default.
- W1990975553 hasConcept C54355233 @default.
- W1990975553 hasConcept C552990157 @default.
- W1990975553 hasConcept C86803240 @default.
- W1990975553 hasConcept C8891405 @default.
- W1990975553 hasConcept C90375314 @default.
- W1990975553 hasConceptScore W1990975553C134935766 @default.
- W1990975553 hasConceptScore W1990975553C143425029 @default.
- W1990975553 hasConceptScore W1990975553C153911025 @default.
- W1990975553 hasConceptScore W1990975553C203014093 @default.
- W1990975553 hasConceptScore W1990975553C2776090121 @default.
- W1990975553 hasConceptScore W1990975553C2778378917 @default.
- W1990975553 hasConceptScore W1990975553C2780252810 @default.
- W1990975553 hasConceptScore W1990975553C54355233 @default.
- W1990975553 hasConceptScore W1990975553C552990157 @default.
- W1990975553 hasConceptScore W1990975553C86803240 @default.
- W1990975553 hasConceptScore W1990975553C8891405 @default.
- W1990975553 hasConceptScore W1990975553C90375314 @default.
- W1990975553 hasIssue "2" @default.
- W1990975553 hasLocation W19909755531 @default.
- W1990975553 hasLocation W19909755532 @default.
- W1990975553 hasOpenAccess W1990975553 @default.
- W1990975553 hasPrimaryLocation W19909755531 @default.
- W1990975553 hasRelatedWork W1991644354 @default.
- W1990975553 hasRelatedWork W2004480716 @default.
- W1990975553 hasRelatedWork W2033918102 @default.
- W1990975553 hasRelatedWork W2055890925 @default.
- W1990975553 hasRelatedWork W2107516157 @default.