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1.

001-es BibID:BIBFORM005805
Első szerző:Glant Tibor T.
Cím:Two loci on chromosome 15 control experimentally induced arthritis through the differential regulation of IL-6 and lymphocyte proliferation / Tibor T. Glant, Sandor Szanto, Aniko Vegvari, Zoltan Szabo, Katalin Kis-Toth, Katalin Mikecz, Vyacheslav A. Adarichev
Dátum:2008
Megjegyzések:Using genetic linkage analysis of proteoglycan-induced arthritis (PGIA), a murine model for rheumatoid arthritis, we identified two loci, Pgia8 and Pgia9, on chromosome 15 (chr15) that appear to be implicated in disease susceptibility. Immunization of congenic strains carrying the entire chr15 and separately each of the two loci of DBA/2 arthritis-resistant origin in susceptible BALB/c background confirmed locations of two loci on chr15: the major Pgia9 and lesser Pgia8 locus. Distal part of chr15 (Pgia9) showed a major suppressive effect on PGIA susceptibility in females (40%, p < 0.001), whereas the effect of this locus in congenic males was still significant but weaker. Proximal part of chr15 (Pgia8) demonstrated mild and transient effect upon arthritis; this effect was PGIA-promoting in males and suppressive in females. Pgia8 and Pgia9 loci demonstrated an additive mode of inheritance, since when they were both incorporated in consomic chr15 strain, the total effect was a sum of the two loci. Using F-2 population of the intercross of wild-type and chr15 consomic strain, we confirmed and refined quantitative trait locus positions and identified a strong correlation between disease susceptibility and lymphocyte-producing cytokines of TNF-alpha and IL-6. Both Pgia8 and Pgia9 loci on chr15 appear to control IL-6 production in spleen cultures of arthritic mice, providing an important link to the mechanism of autoimmune inflammation.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Collagen-induced arthritis
Quantitative trait loci
Proteoglycan-induced arthritis
Rheumatoid-arthritis
Susceptibility loci
Genome scan
Genetic dissection
Autoimmune-disease
Murine model
Identification
Megjelenés:The Journal of Immunology. - 181 : 2 (2008), p. 1307-1314. -
További szerzők:Szántó Sándor (1968-) (belgyógyász, reumatológus) Végvári Anikó (belgyógyász, III. sz. Belgyógyászati Klinika) Szabó Zoltán (1970-) (belgyógyász, reumatológus) Kis-Tóth Katalin (1975-) (immunológus) Mikecz Katalin Adarichev, Vyacheslav A.
Internet cím:elektronikus 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
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3.

001-es BibID:BIBFORM028771
Első szerző:Révészné Tóth Réka (molekuláris biológus, biokémikus)
Cím:Activation-induced apoptosis and cell surface expression of Fas (CD95) ligand are reciprocally regulated by retinoic acid receptor alpha and gamma and involve nur77 in T cells / Réka Tóth, Éva Szegezdi, Uwe Reichert, Jean-Michel Bernardon, Serge Michel, Philippe Ancian, Katalin Kis-Tóth, Zsolt Macsári, László Fésüs, Zsuzsa Szondy
Dátum:2001
ISSN:0014-2980
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:European Journal of Immunology. - 31 : 5 (2001), p. 1382-1391. -
További szerzők:Szegezdi Éva Reichert, Uwe Bernardon, Jean Michel Michel, Serge Ancian, Philippe Kis-Tóth Katalin (1975-) (immunológus) Macsári Zsolt Fésüs László (1947-) (orvos biokémikus) Szondy Zsuzsanna (1959-) (molekuláris sejtbiológus, biokémikus)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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4.

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)
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DOI
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