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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
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DOI
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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.
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DOI
Intézményi repozitóriumban (DEA) tárolt változat
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