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001-es BibID:	BIBFORM055554
Első szerző:	Pázmándi Kitti Linda (molekuláris biológus, immunológus)
Cím:	Oxidative modification enhances the immunostimulatory effects of extracellular mitochondrial DNA on plasmacytoid dendritic cells / Kitti Pazmandi, Zsofia Agod, Brahma V. Kumar, Attila Szabo, Tunde Fekete, Viktoria Sogor, Agota Veres, Istvan Boldogh, Eva Rajnavolgyi, Arpad Lanyi, Attila Bacsi
Dátum:	2014
ISSN:	0891-5849
Megjegyzések:	Inflammation is associated with oxidative stress and characterized by elevated levels of damage-associated molecular pattern (DAMP) molecules released from injured or even living cells into the surrounding microenvironment. One of these endogenous danger signals is the extracellular mitochondrial DNA (mtDNA) containing evolutionary conserved unmethylated CpG repeats. Increased levels of reactive oxygen species (ROS) generated by recruited inflammatory cells modify mtDNA oxidatively resulting primarily in accumulation of 8-oxo-7,8-dihydroguanine (8-oxoG) lesions. In this study, we examined the impact of native and oxidatively modified mtDNAs on the phenotypic and functional properties of plasmacytoid dendritic cells (pDCs), which possess a fundamental role in the regulation of inflammation and T cell immunity. Treatment of human primary pDCs with native mtDNA up-regulated the expression of a co-stimulatory molecule (CD86), a specific maturation marker (CD83), and a main antigen-presenting molecule (HLA-DQ) on the cell surface, as well as increased TNF-? and IL-8 production from the cells. These effects were more apparent when pDCs were exposed to oxidatively modified mtDNA. Neither native nor oxidized mtDNA molecules were able to induce interferon (IFN)-? secretion from pDCs unless they formed a complex with human cathelicidin LL-37, an antimicrobial peptide. Interestingly, simultaneous administration of a Toll-like receptor (TLR)9 antagonist abrogated the effects of both native and oxidized mtDNAs on human pDCs. In a murine model, oxidized mtDNA also proved a more potent activator of pDCs compared to the native form, except for induction of IFN-? production. Collectively, we demonstrate here for the first time that elevated levels of 8-oxoG bases in the extracellular mtDNA induced by oxidative stress increase the immunostimulatory capacity of mtDNA on pDCs.
Tárgyszavak:	Természettudományok Biológiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban Plasmacytoid dendritic cells Extracellular mitochondrial DNA Oxidative stress 8-oxoguanine base Inflammation
Megjelenés:	Free Radical Biology and Medicine. - 77 (2014), p. 281-290. -
További szerzők:	Agod Zsófia Kumar, Brahma V. Szabó Attila (1981-) (molekuláris biológus, immunológus, filozófus) Fekete Tünde (1984-) (immunológus, molekuláris biológus, mikrobiológus) Somogyi Viktória (1989-) (biotechnológus) Veres Ágota (laboráns) Boldogh István Rajnavölgyi Éva (1950-) (immunológus) Lányi Árpád (1962-) (biológus, immunológus) Bácsi Attila (1967-) (immunológus)
Pályázati támogatás:	K-109595 OTKA TAMOP-4.2.2.A-11/1/KONV-2012-0023 TÁMOP
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001-es BibID:	BIBFORM030562
Első szerző:	Pázmándi Kitti Linda (molekuláris biológus, immunológus)
Cím:	Modulatory effects of low-dose hydrogen peroxide on the function of human plasmacytoid dendritic cells / Kitti Pazmandi, Zoltan Magyarics, Istvan Boldogh, Aniko Csillag, Eva Rajnavolgyi, Attila Bacsi
Dátum:	2012
ISSN:	0891-5849
Megjegyzések:	Under normal conditions, plasmacytoid dendritic cells (pDCs) are located in peripheral lymphoid organs or circulate in the blood, from where they can migrate to sites of infection or inflammation. In inflamed tissues, pDCs can be exposed to elevated levels of reactive oxygen species produced by inflammatory cells and we presume that oxidative stress could affect the cellular responses of pDCs to microenvironmental stimuli. To explore this possibility, human pDCs isolated from peripheral blood of healthy donors were treated with H(2)O(2) and R837 (a Toll-like receptor 7 ligand), separately and in combination. Our results demonstrate that treatment with a low concentration (0.01?M) of H(2)O(2) resulted in only slight changes in the expression of CD40, CD80, CD86, and CD83; however, low-dose H(2)O(2) markedly decreased the expression of HLA-DQ on pDCs. Exposure to H(2)O(2) did not trigger the release of IL-6, TNF-?, IL-8, or IFN-? from pDCs. Although addition of H(2)O(2) did not modify the capacity of pDCs to activate allogeneic IL-17- or IFN-?-producing T cells, it significantly increased the ability of pDCs to stimulate IL-4-secreting T cells. Exposure of pDCs to H(2)O(2) before cocultivation with naïve autologous T cells significantly lowered IL-10 production by T cells, but did not affect IL-17 release. It was also observed that H(2)O(2)-exposed pDCs provided stronger stimuli for Th2 than for Th1 differentiation upon autologous activation, compared to untreated pDCs, possibly because of elevated surface expression of OX40-L. Most importantly, when pDCs were stimulated with R837 in the presence of H(2)O(2), decreased phenotypic activation, decreased chemokine and cytokine release, and impaired allo- and autostimulatory functions of pDCs were detected, indicating that pDCs exposed to oxidative stress in vivo may have an anti-inflammatory or tolerogenic role in regulating adaptive immune responses.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Molekuláris Medicina Plasmacytoid dendritic cells Oxidative stress Inflammation Immune regulation Free radicals egyetemen (Magyarországon) készült közlemény
Megjelenés:	Free Radical Biology and Medicine 52 : 3 (2012), p. 635-645. -
További szerzők:	Magyarics Zoltán (1982-) (immunológus) Boldogh István Csillag Anikó (1979-) (immunológus, biológus, angol-magyar szakfordító) Rajnavölgyi Éva (1950-) (immunológus) Bácsi Attila (1967-) (immunológus)
Pályázati támogatás:	TÁMOP-4.2.1/B-09/1/KONV-2010-0007 TÁMOP Molekuláris immunológia
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001-es BibID:	BIBFORM037368
Első szerző:	Robaszkiewicz, Agnieszka (biokémikus)
Cím:	Hydrogen peroxide-induced poly(ADP-ribosyl)ation regulates osteogenic differentiation-associated cell death / Robaszkiewicz Agnieszka, Erdélyi Katalin, Kovács Katalin, Kovács István, Bai Péter, Rajnavölgyi Éva, Virág László
Dátum:	2012
ISSN:	0891-5849
Megjegyzések:	We set out to investigate the role of poly(ADP-ribosylation), the attachment of NAD(+)-derived (ADP-ribose)(n) polymers to proteins, in the regulation of osteogenic differentiation of SAOS-2 cells and mesenchymal stem cells. In osteogenic differentiation medium, SAOS-2 cells showed mineralization and expressed alkaline phosphatase and osteoblastic marker genes such as Runx2, osterix, BMP2, and osteopontin. The cells also released hydrogen peroxide, displayed poly(ADP-ribose) polymerase (PARP) activation, and showed commitment to cell death (apoptosis and necrosis). Scavenging reactive oxygen species by glutathione or decomposing hydrogen peroxide by the addition of catalase reduced differentiation, PARP activation, and cell death. We silenced the expression of the main PAR-synthesizing enzyme PARP-1 and the PAR-degrading enzyme poly(ADP-ribose) glycohydrolase (PARG) in SAOS-2 osteosarcoma cells (shPARP-1 and shPARG, respectively). Both shPARP-1- and shPARG-silenced cells exhibited altered differentiation, with the most notable change being increased osteopontin expression but decreased alkaline phosphatase activity. PARP-1 silencing suppressed both apoptotic and necrotic cell death, but the PARP inhibitor PJ34 sensitized cells to cell death, indicating that the effects of PARP-1 silencing are not related to the activity of the enzyme. PARG silencing resulted in more apoptosis and, in the last days of differentiation, a shift from apoptosis toward necrosis. In conclusion our data prove that hydrogen peroxide-induced poly(ADP-ribose) signaling regulates cell death and osteodifferentiation.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Molekuláris Medicina
Megjelenés:	Free Radical Biology And Medicine. - 53 : 8 (2012), p. 1552-1564. -
További szerzők:	Erdélyi Katalin (1978-) (molekuláris biológus, biokémikus) Kovács Katalin (1978-) (biokémikus) Kovács István (1985-) (biokémikus) Bai Péter (1976-) (biokémikus) Rajnavölgyi Éva (1950-) (immunológus) Virág László (1965-) (biokémikus, sejtbiológus, farmakológus)
Pályázati támogatás:	K82009 OTKA K75864 OTKA PD83473 OTKA TÁMOP-4.2.2.A-11/1/KONV-2012-0025 TÁMOP TÁMOP-4.2.1/B-09/1/KONV-2010-0007 TÁMOP Oxidatív stressz és ADP-riboziláció kapcsolatának vizsgálata TÁMOP-4.2.1/B-09/1/KONV-2010-0007 TÁMOP Jelátviteli kapcsolatok ős- és dendritikus sejt altípusokban TÁMOP-4.2.2/B-10/1-2010-0024 TÁMOP
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