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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
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
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2.

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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3.

001-es BibID:BIBFORM010313
Első szerző:Zsíros Emese (orvos)
Cím:Developmental switch of the expression of ion channels in human dendritic cells / Zsiros Emese, Kis-Tóth Katalin, Hajdú Péter, Gáspár Rezső, Joanna Bielansk, Antonio Felipe, Rajnavölgyi Éva, Panyi György
Dátum:2009
ISSN:0022-1767
Megjegyzések:Modulation of the expression and activity of plasma membrane ion channels is one of the mechanisms by which immune cells can regulate their intracellular Ca2(+) signaling pathways required for proliferation and/or differentiation. Voltage-gated K+ channels, inwardly rectifying K+ channels, and Ca2+-activated K+ channels have been described to play a major role in controlling the membrane potential in lymphocytes and professional APCs, such as monocytes, macrophages, and dendritic cells (DCs). Our study aimed at the characterization and identification of ion channels expressed in the course of human DC differentiation from monocytes. We report in this study for the first time that immature monocyte-derived DCs express voltage-gated Na+ channels in their plasma membrane. The analysis of the biophysical and pharmacological properties of the current and PCR-based cloning revealed the presence of Nav1.7 channels in immature DCs. Transition from the immature to a mature differentiation state, however, was accompanied by the down-regulation of Nav1.7 expression concomitant with the up-regulation of voltage-gated Kv1.3 K+ channel expression. The presence of Kv1.3 channels seems to be common for immune cells; hence, selective Kv1.3 blockers may emerge as candidates for inhibiting various functions of mature DCs that involve their migratory, cytokine-secreting, and T cell-activating potential.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Union of Pharmacology
Dependent K+ channel
Human Lymhocytes T
Potassium channels
Sodium Channels
Electrophysiological properties
Peripheral nerve
Immune system
Macrophages
Activation
Megjelenés:The Journal of Immunology 183 : 7 (2009), p. 4483-4492. -
További szerzők:Kis-Tóth Katalin (1975-) (immunológus) Hajdu Péter (1975-) (biofizikus) Gáspár Rezső (1944-) (biofizikus) Bielansk, Joanna Felipe, Antonio Rajnavölgyi Éva (1950-) (immunológus) Panyi György (1966-) (biofizikus)
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
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