Összesen 6 találat.


001-es BibID:BIBFORM020146
Első szerző:Altorjay István (belgyógyász, gasztroenterológus, onkológus)
Cím:Anti-TNF-alpha antibody (infliximab) therapy supports the recovery of eNOS and VEGFR2 protein expression in endothelial cells / Istvan Altorjay, Zoltan Vereb, Zoltan Serfozo, Ildiko Bacskai, Robert Batori, Ferenc Erdodi, Miklos Udvardy, Sandor Sipka, Arpad Lanyi, Eva Rajnavolgyi, Karoly Palatka
Megjegyzések:The aim of this study is to investigate the effect of sera obtained from patients of Crohn's disease treated by anti-TNF-alpha antibody (infliximab) on the expression of endothelial nitric oxide synthase (eNOS) and vascular endothelial growth factor receptor-2 (VEGFR2) protein in human umbilical vein endothelial cells (HUVEC) cultured in vitro. HUVEC was cultured in the presence of sera derived from patients before and after treatment, or from healthy individuals. Effects of sera on the expression of eNOS and VEGFR2 were monitored by determination of mRNA and protein levels using real time quantitative PCR and Western blot analysis, respectively. The serum of Crohn's patients contained elevated levels of TNF-alpha (34 +/- 1.80 pg/mL), which resulted in a decrease in the protein level of eNOS in HUVEC with a simultaneous induction of VEGFR2. Infliximab treatment normalized the expression level of these proteins by decreasing TNF-alpha level, particularly in those cases when clinical healing was also recorded, and it also conferred restitution of the level of angiogenic cytokines. Results suggest that altered angiogenesis possibly contributes to the initiation and perpetuation of inflammatory processes in Inflammatory Bowel Disease (IBD). Endothelial dysfunction, a selective feature of Crohn's disease is beneficially affected by intravascular TNF-alpha neutralization.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Crohn's disease
inflammatory bowel disease
Vascular endothelial growth factor receptor-2
Megjelenés:International Journal of Immunopathology and Pharmacology 24 : 2 (2011), p. 323-335. -
További szerzők:Veréb Zoltán (1980-) (immunológus, mikrobiológus, molekuláris biológus) Serfőző Zoltán Bacskai Ildikó (1985-) (immunológus) Bátori Róbert Károly (1983-) (biológus, biotechnológus) Erdődi Ferenc (1953-) (biokémikus) Udvardy Miklós (1947-) (belgyógyász, haematológus) Sipka Sándor (1945-) (laboratóriumi szakorvos) Lányi Árpád (1962-) (biológus, immunológus) Rajnavölgyi Éva (1950-) (immunológus) Palatka Károly (1961-) (belgyógyász, gasztroenterológus)
Pályázati támogatás:0046/NA/2006-2/OP-9
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001-es BibID:BIBFORM058666
Első szerző:Bacskai Ildikó (immunológus)
Cím:Mesenchymal stromal cell-like cells set the balance of stimulatory and inhibitory signals in monocyte-derived dendritic cells / Ildikó Bacskai, Anett Mázló, Katalin Kis-Tóth, Attila Szabó, György Panyi, Balázs Sarkadi, Ágota Apáti, Éva Rajnavölgyi
Megjegyzések:The major reservoir of human multipotent mesenchymal stem/stromal cells (MSC) is the bone marrow (BM) with the capability to control hematopoietic stem cell (HSC) development. The regenerative potential of MSC is associated with enhanced endogenous repair and healing mechanisms that modulate inflammatory responses. Our previous results revealed that MSC-like (MSCl) cells derived from pluripotent human embryonic stem cells resemble BM-derived MSC in morphology, phenotype and differentiating potential. Here we investigated the effects of MSCl cells on the phenotype and functions of dendritic cells (DC). To assess how anti-viral immune responses could be regulated by intracellular pattern recognition receptors (PRR) of DC in the presence of MSCl cells we activated DC with the specific ligands of retinoic acid-inducible gene I (RIG-I) helicases and found that activated DC co-cultured with MSCl cells exhibited reduced expression of CD1a and CD83 cell surface molecules serving as phenotypic indicators of DC differentiation and activation, respectively. However, RIG-I-mediated stimulation of DC via specific ligands in the presence of MSCl cells resulted in significantly higher expression of the co-stimulatory molecules CD80 and CD86 than in the presence of BM-MSC. In line with these results the concentration of IL-6, IL-10 and CXCL8 was increased in the supernatant of the DC-MSCl co-cultures, while the secretion of TNF-?, CXCL10, IL-12 and IFN? was reduced. Furthermore, the concerted action of mechanisms involved in the regulation of DC migration resulted in the blockade of cell migration indicating altered DC functionality mediated by MSCl cell-derived signals and mechanisms resulting in a suppressive microenvironment.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
mesenchymal stromal cell
dendritic cell
RIG-like receptors
matrix metalloproteinases
Megjelenés:Stem Cells And Development. - 24 : 15 (2015), p. 1805-1816. -
További szerzők:Türk-Mázló Anett (1989-) (molekuláris biológus) Kis-Tóth Katalin (1975-) (immunológus) Szabó Attila (1981-) (molekuláris biológus, immunológus, filozófus) Panyi György (1966-) (biofizikus) Sarkadi Balázs Apáti Ágota Rajnavölgyi Éva (1950-) (immunológus)
Pályázati támogatás:TÁMOP 4.2.4. A/2-11-1-2012-0001
TÁMOP 4.2.2.A-11/1/KONV-2012-0023
OTKA NK 101538
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001-es BibID:BIBFORM049592
035-os BibID:PMID:23870824
Első szerző:Kis-Tóth Katalin (immunológus)
Cím:Monocyte-derived dendritic cell subpopulations use different types of matrix metalloproteinases inhibited by GM6001 / Katalin Kis-Toth, Ildiko Bacskai, Peter Gogolak, Anett Mazlo, Istvan Szatmari, Eva Rajnavolgyi
Megjegyzések:Matrix metalloproteinases (MMPs) are endopeptidases with the potential to cleave extracellular matrix, support tissue renewal and regulate cell migration. Functional activities of MMPs are regulated by tissue inhibitors of MMPs (TIMPs) and disruption of the MMP-TIMP balance has pathological consequences. Here we studied the expression and secretion of MMPs and TIMPs in CD1a(-) and CD1a(+) monocyte-derived dendritic cell (DC) subpopulations. Our results showed that monocytes express TIMPs but lack MMPs, whereas upon differentiation to moDCs and in response to activation signals the expression of MMPs is increased and that of TIMPs is decreased. MMP-9 is expressed dominantly in the CD1a(-) subpopulation, while MMP-12 is preferentially expressed in CD1a(+) cells. Experiments performed with the synthetic MMP inhibitor GM6001 revealed that this drug efficiently inhibits the migration of moDCs through inactivation of MMPs. We conclude that modulation of MMP activity by GM6001 emerges as a novel approach to manipulate DC migration under inflammatory conditions. (C) 2013 Elsevier GmbH. All rights reserved.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Dendritic cell
Matrix metalloproteinase
Tissue inhibitor of matrix
Megjelenés:Immunobiology. - 218 : 11 (2013), p. 1361-1369. -
További szerzők:Bacskai Ildikó (1985-) (immunológus) Gogolák Péter (1968-) (biológus, immunológus) Türk-Mázló Anett (1989-) (molekuláris biológus) Szatmári István (1971-) (biológus) Rajnavölgyi Éva (1950-) (immunológus)
Pályázati támogatás:TÁMOP-4.2.2.A-11/1/KONV-2012-0023-"VÉD-ELEM"
NK 101538
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001-es BibID:BIBFORM020764
Első szerző:Kis-Tóth Katalin (immunológus)
Cím:Voltage-Gated Sodium Channel Nav1.7 Maintains the Membrane Potential and Regulates the Activation and Chemokine-Induced Migration of a Monocyte-Derived Dendritic Cell Subset / Katalin Kis-Toth, Peter Hajdu, Ildiko Bacskai, Orsolya Szilagyi, Ferenc Papp, Attila Szanto, Edit Posta, Peter Gogolak, Gyorgy Panyi, Eva Rajnavolgyi
Megjegyzések:Expression of CD1a protein defines a human dendritic cell (DC) subset with unique functional activities. We aimed to study the expression of the Nav1.7 sodium channel and the functional consequences of its activity in CD1a(-) and CD1a(+) DC. Single-cell electrophysiology (patch-clamp) and quantitative PCR experiments performed on sorted CD1a(-) and CD1a(+) immature DC (IDC) showed that the frequency of cells expressing Na(+) current, current density, and the relative expression of the SCN9A gene encoding Nav1.7 were significantly higher in CD1a(+) cells than in their CD1a(-) counterparts. The activity of Nav1.7 results in a depolarized resting membrane potential (-8.7 +/- 1.5 mV) in CD1a(+) IDC as compared with CD1a(-) cells lacking Nav1.7 (-47 +/- 6.2 mV). Stimulation of DC by inflammatory signals or by increased intracellular Ca(2+) levels resulted in reduced Nav1.7 expression. Silencing of the SCN9A gene shifted the membrane potential to a hyperpolarizing direction in CD1a(+) IDC, resulting in decreased cell migration, whereas pharmacological inhibition of Nav1.7 by tetrodotoxin sensitized the cells for activation signals. Fine-tuning of IDC functions by a voltage-gated sodium channel emerges as a new regulatory mechanism modulating the migration and cytokine responses of these DC subsets
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:The Journal of Immunology. - 187 : 3 (2011), p. 1273-1280. -
További szerzők:Hajdu Péter (1975-) (biofizikus) Bacskai Ildikó (1985-) (immunológus) Szilágyi Orsolya (1985-) (molekuláris biológus, biokémikus) Papp Ferenc (1979-) (biofizikus) Szántó Attila (1976-) (orvos, biokémikus) Feketéné Posta Edit (1986-) (reumatológus) Gogolák Péter (1968-) (biológus, immunológus) Panyi György (1966-) (biofizikus) Rajnavölgyi Éva (1950-) (immunológus)
Pályázati támogatás:TÁMOP-4.2.1/B-09/1/KONV-2010-0007
Molekuláris immunológia
Internet cím:DOI
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001-es BibID:BIBFORM037289
Első szerző:Szabó Attila (molekuláris biológus, immunológus, filozófus)
Cím:Temporally designed treatment of melanoma cells by ATRA and polyI:C results in enhanced chemokine and IFNb secretion controlled differently by TLR3 and MDA5 / Szabo Attila, Osman Rolah M., Bacskai Ildiko, Kumar Brahma V., Agod Zsofia, Lanyi Arpad, Gogolak Peter, Rajnavolgyi Eva
Megjegyzések:In the last three decades, the incidence of melanoma has increased worldwide and no effective treatment modalities have been developed yet. All-trans retinoic acid (ATRA) and polyinosinic:polycytidylic acid (polyI:C) are strong inducers of toll-like receptor 3 (TLR3) and MDA5 expression, and polyI:C-induced TLR3 and MDA5 signaling specifically causes cell death in melanoma cells in vitro. We addressed the question of whether ATRA pretreatment could enhance the efficacy of polyI:C and, if so, would ATRA have any additional effects on this process. We found that the combined treatment of human melanoma cells with ATRA and polyI:C strongly increased the expression of TLR3 and MDA5 in both WM35 and WM983A cells associated with significantly higher mRNA and secreted levels of interferon b (IFNb), CXCL1, CXCL8/IL-8, CXCL9, and CXCL10 than cells treated with either ATRA or polyI:C. Silencing of MDA5 by siRNA moderately affected IFNb secretion, whereas TLR3 knockdown interfered with both CXCL chemokine and IFNb production. Furthermore, the supernatants of ATRA + polyI:C-activated cultures increased the migration of both human monocyte-derived macrophages and CD1a + dendritic cells significantly as compared with the supernatants of cells treated with either ATRA or polyI:C, and this effect occurred in a TLR3-dependent manner. In conclusion, consecutive treatment with ATRA and polyI:C results in strong, TLR3/MDA5-mediated chemokine and IFN responses in cultured human melanoma cells, which triggers a functional migratory response in professional antigen-presenting cells. This novel mode of concomitant activation may represent a more efficient treatment option for future melanoma therapy.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Molekuláris Medicina
Megjelenés:Melanoma Research 22 : 5 (2012), p. 351-361. -
További szerzők:Osman, Rolah M. Bacskai Ildikó (1985-) (immunológus) Kumar, Brahma V. Agod Zsófia Lányi Árpád (1962-) (biológus, immunológus) Gogolák Péter (1968-) (biológus, immunológus) Rajnavölgyi Éva (1950-) (immunológus)
Pályázati támogatás:TÁMOP-4.2.1/B-09/1/KONV-2010-0007
Jelátviteli kapcsolatok ős- és dendritikus sejt altípusokban
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001-es BibID:BIBFORM093554
035-os BibID:(cikkazonosító)102312 (WoS)000642261700061 (Scopus)85103387106
Első szerző:Türk-Mázló Anett (molekuláris biológus)
Cím:MSC-like cells increase ability of monocyte-derived dendritic cells to polarize IL-17-/IL-10-producing T cells via CTLA-4 / Mázló Anett, Kovács Ramóna, Miltner Noémi, Tóth Márta, Veréb Zoltán, Szabó Krisztina, Bacskai Ildikó, Pázmándi Kitti, Apáti Ágota, Bíró Tamás, Bene Krisztián, Rajnavölgyi Éva, Bácsi Attila
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:iScience. - 24 : 4 (2021), p. 1-25. -
További szerzők:Kovács Ramóna (1991-) (biológus, okleveles klinikai laboratóriumi kutató) Miltner Noémi (1990-) (molekuláris biológus) Tóth Márta (1986-) (biológus) Veréb Zoltán (1980-) (immunológus, mikrobiológus, molekuláris biológus) Szabó Krisztina (1987-) (Molekuláris biológus) Bacskai Ildikó (1985-) (immunológus) Pázmándi Kitti Linda (1984-) (molekuláris biológus, immunológus) Apáti Ágota Bíró Tamás (1968-) (élettanász) Bene Krisztián (1986-) (Biológus) Rajnavölgyi Éva (1950-) (immunológus) Bácsi Attila (1967-) (immunológus)
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