CCL

Összesen 5 találat.
#/oldal:
Részletezés:
Rendezés:

1.

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)
Internet cím:elektronikus változat
DOI
Borító:

2.

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

3.

001-es BibID:BIBFORM065602
Első szerző:Ludányi Katalin (immunológus)
Cím:Fine-tuning of helper T cell activation and apoptosis by antigen-presenting cells / Katalin Ludanyi, Peter Gogolak, Bence Rethi, Maria Magocsi, Cynthia Detre, Janos Matko Eva Rajnavolgyi
Dátum:2004
ISSN:0898-6568
Megjegyzések:The role of antigen-presenting cells (APC) in regulating helper T cell responses and activation-induced cell death (AICD) was investigated in vitro. T cell activation was monitored by measuring the early rise of intracellular free calcium [Ca+]ic, mRNA and cell surface expression of activation and apoptotic molecules, the production of cytokines and the activation of transcription factors. Our results demonstrate that the unique characteristics of a given APC can modify the threshold, kinetics and magnitude of the T cell response. The rapid and sustained rise of intracellular free calcium correlated well with the extent of cytokine production and the expression of activation molecules. Fas-dependent AICD could be induced by the most potent antigen-presenting cell (2PK3) only. Our results demonstrate that the response and fate of effector/memory CD4+ helper T lymphocytes is highly dependent on the individual properties of the APC they encounter.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
APC
Antigen presentation
TCR
Co-stimulation
T cell signaling
Antigen-specific activation
Helper T cell
AICD
Megjelenés:Cellular Signalling. - 16 : 8 (2004), p. 939-950. -
További szerzők:Gogolák Péter (1968-) (biológus, immunológus) Réthi Bence (1973-) (biológus, immunológus) Magócsi Mária Detre, Cynthia Matkó János (1952-) (biológus) Rajnavölgyi Éva (1950-) (immunológus)
Pályázati támogatás:T043420
OTKA
NKFP 00088/2001
Egyéb
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

4.

001-es BibID:BIBFORM065587
Első szerző:Rajnavölgyi Éva (immunológus)
Cím:IL-7 withdrawal induces a stress pathway activating p38 and Jun N-terminal kinases / Eva Rajnavolgyi, Naima Benbernou, Bence Rethi, Della Reynolds, Howard A. Young, Maria Magocsi, Kathrin Muegge, Scott K. Durum
Dátum:2002
ISSN:0898-6568
Megjegyzések:IL-7 delivers survival signals to cells at an early stage in lymphoid development. In the absence of IL-7, pro-T cells undergo programmed cell death, which has previously been associated with a decline in Bcl-2 and translocation of Bax from cytosol to mitochondria. A new, earlier feature of IL-7 withdrawal was identified using an IL-7-dependent thymocyte line. We observed that withdrawal of IL-7 induced increased expression of jun and fos family member genes including c-jun, junB, junD, c-fos and fra2. This transient response peaked 3-4 h after IL-7 was withdrawn and resulted in increased DNA-binding activity of AP-1 and in a change in the composition of the Jun/Fos family dimers shown by electrophoretic mobility shift and supershift assays. Induction of jun and fos genes and the increased DNA-binding activity of AP-1 were attributable to the phosphorylation-induced activation of the stress kinases p38 and JNK and were blocked by the chemical kinase inhibitors SB203580 and SB202190. The stress response contributed to cell death following IL-7 withdrawal as shown by blocking the activity of the stress (MAP) kinases or by blocking the production of c-Jun and c-Fos using antisense oligonucleotides.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Apoptosis
Cell death
Interleukin-7
jun
fos
MAP kinase
Lymphocyte
Stress
Megjelenés:Cellular Signalling 14 : 9 (2002), p. 761-769. -
További szerzők:Benbernou, Naima Réthi Bence (1973-) (biológus, immunológus) Reynolds, Della Young, Howard A. Magócsi Mária Muegge, Kathrin Durum, Scott K.
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

5.

001-es BibID:BIBFORM063227
Első szerző:Szabó Attila (molekuláris biológus, immunológus, filozófus)
Cím:RIG-I inhibits the MAPK-dependent proliferation of BRAF mutant melanoma cells via MKP-1 / Attila Szabo, Tunde Fekete, Gabor Koncz, Brahma V. Kumar, Kitti Pazmandi, Zsofia Foldvari, Balazs Hegedus, Tamas Garay, Attila Bacsi, Eva Rajnavolgyi, Arpad Lanyi
Dátum:2016
ISSN:0898-6568
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
RIG-I
PRR
MAPK
Interferon
Melanoma
Proliferation
Megjelenés:Cellular Signalling 28 : 5 (2016), p. 335-347. -
További szerzők:Fekete Tünde (1984-) (immunológus, molekuláris biológus, mikrobiológus) Koncz Gábor (1970-) (biológus, immunológus) Kumar, Brahma V. Pázmándi Kitti Linda (1984-) (molekuláris biológus, immunológus) Földvári Zsófia Hegedűs Balázs Garay Tamás Bácsi Attila (1967-) (immunológus) Rajnavölgyi Éva (1950-) (immunológus) Lányi Árpád (1962-) (biológus, immunológus)
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Rekordok letöltése1 
Corvina könyvtári katalógus v8.2.27 © 2023 Monguz kft. Minden jog fenntartva.