CCL

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1.

001-es BibID:BIBFORM086399
Első szerző:Detre, Cynthia
Cím:Dual face of ceramide : non-apoptotic Cer-stimuli modulate antigen-specific T-cell activation through blocking plasma membrane ion channels / Detre C., Kiss E., Varga Zoltán, Ludányi Katalin, Pászty K., Enyedi Á., Panyi György, Rajnavölgyi Éva, Matkó János
Dátum:2005
ISSN:1742-464X
Tárgyszavak:Orvostudományok Klinikai orvostudományok idézhető absztrakt
folyóiratcikk
Megjelenés:Febs Journal. - 272 : Suppl1 (2005), p. 193. -
További szerzők:Kiss E. Varga Zoltán (1969-) (biofizikus, szakfordító) Ludányi Katalin (1975-) (immunológus) Pászty Katalin Enyedi Ágnes Panyi György (1966-) (biofizikus) Rajnavölgyi Éva (1950-) (immunológus) Matkó János (1952-) (biológus)
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2.

001-es BibID:BIBFORM005082
Első szerző:Detre, Cynthia
Cím:Death or survival : membrane ceramide controls the fate and activation of antigen-specific T-cells depending on signal strength and duration / Detre, C., Kiss, E., Varga, Z., Ludanyi, K., Paszty, K., Enyedi, A., Kovesdi, D., Panyi, G., Rajnavolgyi, E., Matko, J.
Dátum:2006
ISSN:898-6568 (Print)
Megjegyzések:Sphingomyelinase (SMase)-mediated release of ceramide in the plasma membrane of T-lymphocytes induced by different stimuli such as ligation of Fas/CD95, irradiation, stress, inflammation or anticancer drugs primarily involves mitochondrial apoptosis signaling, but under specific conditions non-apoptotic Fas-signaling was also reported. Here we investigated, using a quantitative simulation model with exogenous C2-ceramide (and SMase), the dependence of activation and fate of T-cells on the strength and duration of ceramide accumulation. A murine, influenza virus hemagglutinin-specific T-helper cell (IP12-7) alone or together with interacting antigen presenting B-cells (APC) was used. C2-ceramide induced apoptosis of TH cells above a 'threshold' stimulus (>25 microM in 'strength' or >30 min in duration), while below the threshold C2-ceramide was non-apoptotic, as confirmed by early and late apoptotic markers (PS-translocation, mitochondrial depolarization, caspase-3 activation, DNA-fragmentation). The modest ceramide stimuli strongly suppressed the calcium response and inhibited several downstream signal events (e.g. ERK1/2-, JNK-phosphorylation, CD69 expression or IL-2 production) in TH cells during both anti-CD3 induced and APC-triggered activation. Ceramide moderately affected the Ca2+ -release from internal stores upon antigen-specific engagement of TCR in immunological synapses, while the influx phase was remarkably reduced in both amplitude and rate, suggesting that the major target(s) of ceramide-effects are membrane-proximal. Ceramide inhibited Kv1.3 potassium channels, store operated Ca2+ -entry (SOC) and depolarized the plasma membrane to which contribution of spontaneously formed ceramide channels is possible. The impaired function of these transporters may be coupled to the quantitative, membrane raft-remodeling effect of ceramide and responsible, in a concerted action, for the suppressed activation. Our results suggest that non-apoptotic Fas stimuli, received from previously activated, FasL+ interacting lymphocytes in the lymph nodes, may negatively regulate subsequent antigen-specific T-cell activation and thus modulate the antigen-specific T-cell response.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
analogs and derivatives
Animals
Antigens,CD95
Apoptosis
B-Lymphocytes
Calcium
Caspase 3
Caspases
Cell Membrane
Cell Survival
Cells
DNA Fragmentation
Human
Humans
Hungary
immunology
Inflammation
Interleukin-2
Kv1.3 Potassium Channel
Lymph Nodes
Lymphocyte Activation
Lymphocytes
Membrane Potentials
metabolism
Mice
pharmacology
physiology
Potassium
Potassium Channels
Receptors,Antigen,T-Cell
Research
Signal Transduction
Sphingomyelin Phosphodiesterase
Sphingosine
Support
Synapses
T-Lymphocytes
T-Lymphocytes, Helper-Inducer
Time Factors
Megjelenés:Cellular Signalling. - 18 : 3 (2006), p. 294-306. -
További szerzők:Kiss Endre (Budapest) Varga Zoltán (1969-) (biofizikus, szakfordító) Ludányi Katalin (1975-) (immunológus) Pászty Katalin Enyedi Ágnes Kövesdi Dorottya Panyi György (1966-) (biofizikus) Rajnavölgyi Éva (1950-) (immunológus) Matkó János (1952-) (biológus)
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DOI
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3.

001-es BibID:BIBFORM065603
Első szerző:Kövesdi Dorottya
Cím:Antigen receptor-mediated signaling pathways in transitional immature B cells / Dorottya Kövesdi, Katalin Pászty, Ágnes Enyedi, Endre Kiss, János Matkó, Katalin Ludányi, Éva Rajnavölgyi, Gabriella Sármay
Dátum:2004
ISSN:0898-6568
Megjegyzések:Engagement of antigen receptors on immature B cells induces apoptosis, while at the mature stage, it stimulates cell activation and proliferation. The difference in B cell receptor (BCR)-mediated signaling pathways regulating death or survival of B cells is not fully understood. We aimed to characterize the pathway leading to BCR-driven apoptosis. Transitional immature B cells were obtained from the spleen of sublethally irradiated and auto-reconstituted mice. We have detected a short-lived BCR-driven activation of mitogen-activated protein kinases (ERK1/2 and p38 MAPK) and Akt/PKB in transitional immature B cells that correlated with the lack of c-Fos expression, reduced phosphorylation of Akt substrates and a susceptibility for apoptosis. Simultaneous signaling through BCR and CD40 protected immature B cells from apoptosis, however, without inducing Bcl-2 expression. The BCR-induced apoptosis of immature B cells is a result of the collapse of mitochondrial membrane potential and the subsequent activation of caspase-3.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Apoptosis
B lymphocytes
Development
Signal transduction
Transitional immature cells
Megjelenés:Cellular Signalling. - 16 : 8 (2004), p. 881-889. -
További szerzők:Pászty Katalin Enyedi Ágnes Kiss Endre (Budapest) Matkó János (1952-) (biológus) Ludányi Katalin (1975-) (immunológus) Rajnavölgyi Éva (1950-) (immunológus) Sármay Gabriella
Pályázati támogatás:T029535
OTKA
T034493
OTKA
T034536
OTKA
TS044711
OTKA
D38465
OTKA
FKFP 0155/200
Egyéb
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DOI
Intézményi repozitóriumban (DEA) tárolt változat
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