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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
Dátum:2015
ISSN:1547-3287
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
immunsuppression
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
TÁMOP 4.2.2.A-11/1/KONV-2012-0023
TÁMOP
OTKA NK 101538
OTKA
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DOI
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2.

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
Dátum:2013
ISSN:0171-2985
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
CD1a
Dendritic cell
Immunotherapy
Matrix metalloproteinase
Tissue inhibitor of matrix
Metalloproteinase
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"
TÁMOP
NK 101538
OTKA
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
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3.

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
Dátum:2011
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
ACTIVATION
article
Cells
Electrophysiology
Human
Hungary
immunology
Sodium
Tetrodotoxin
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
TÁMOP
Molekuláris immunológia
TÁMOP-4.2.2-08/1-2008-0015
TÁMOP
Internet cím:DOI
Intézményi repozitóriumban (DEA) tárolt változat
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