Találati lista | Tudóstér

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:
Saját polcon:

001-es BibID:	BIBFORM065601
Első szerző:	Pivarcsi Andor
Cím:	Expression and function of Toll-like receptors 2 and 4 in human keratinocytes / Andor Pivarcsi, Laszlo Bodai, Bence Réthi, Anna Kenderessy-Szabó, Andrea Koreck, Márta Széll, Zsuzsanna Beer, Zsuzsanna Bata-Csörgő, Mária Magócsi, Éva Rajnavölgyi, Attila Dobozy, Lajos Kemény
Dátum:	2003
ISSN:	1460-2377
Megjegyzések:	Keratinocytes have the ability to kill pathogenic fungi and bacteria by producing antimicrobial substances. Recent studies suggest that microbial components use signaling molecules of the human Toll-like receptor (TLR) family to transduce signals in various cells. Here we provide evidence that keratinocytes express both TLR2 and TLR4 at the mRNA and protein levels, and show that TLR2 and TLR4 are present in the normal human epidermis in vivo and that their expression is regulated by microbial components. The expression of myeloid differentiation protein gene (MyD88), which is involved in the signaling pathway of many TLR, was also demonstrated in keratinocytes. LPS + IFN-gamma increased the expression of TLR2 and TLR4 50- and 5-fold respectively. Treatment of keratinocytes with Candida albicans, mannan, Mycobacterium tuberculosis or LPS with IFN-gamma resulted in the activation and nuclear translocation of NF-kappaB. Inhibition of NF-kappaB blocked the Candida-killing activity of keratinocytes, suggesting that the antimicrobial effect of keratinocytes requires NF-kappaB activation. LPS + IFN-gamma, C. albicans (4 Candida/KC), peptidoglycan (1 micro g/ml) or M. tuberculosis extract significantly increased IL-8 gene expression after 3 h of treatment (P < 0.05). The increases over the 0-h level were 15-, 8-, 10.8- and 7-fold, respectively. The microbial compound-induced increase in IL-8 gene expression could be inhibited by anti-TLR2 and anti-TLR4 neutralizing antibodies, suggesting that TLRs are involved in the pathogen-induced expression of this pro-inflammatory cytokine. Our findings stress the importance of the role of keratinocytes as a component of innate immunity.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban epidermis host defense IL-8 innate immunity NF-kB
Megjelenés:	International Immunology 15 : 6 (2003), p. 721-730. -
További szerzők:	Bodai László Réthi Bence (1973-) (biológus, immunológus) Kenderessy Szabó Anna Koreck Andrea Széll Márta Beer Zsuzsanna Bata-Csörgő Zsuzsanna Magócsi Mária Rajnavölgyi Éva (1950-) (immunológus) Dobozy Attila Kemény Lajos
Pályázati támogatás:	T 032496 OTKA T 030749 OTKA T 032498 OTKA T 032494 OTKA FKFP 1271 Egyéb FKFP 0222 Egyéb AKP grant 2000-151 3,2 Egyéb EU5 QLK4-CT2001-00366 Egyéb
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Saját polcon:

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:
Saját polcon:

001-es BibID:	BIBFORM065598
Első szerző:	Réthi Bence (biológus, immunológus)
Cím:	Flow cytometry used for the analysis of calcium signaling induced by antigen-specific T-cell activation / Bence Réthi, Cynthia Detre, Péter Gogolák, Attila Kolonics, Mária Magócsi, Éva Rajnavölgyi
Dátum:	2002
ISSN:	0196-4763
Megjegyzések:	Background: In this study, the effect of antigen-presentingcells (APC), peptide concentration, and CD28 costimulationon calcium signaling, induced by antigen-specificT-cell activation, was studied by flow cytometry.Methods: We used two experimental approaches, whichdiffered in their time scale and in the duration of the Tcell-APC interaction, to measure the increase of intracellularfree calcium levels ([Ca2 ]i) in activated T cells: (1)Fluo-3?loaded T cells were activated by cocentrifugationwith peptide-loaded APC and the kinetics of fluorescenceintensity changes was monitored continuously and (2)peptide-loaded APC and T cells were mixed, cocultured,and the fluorescence intensity was measured at varioustime intervals.Results: The calcium signal of T cells was dependent onthe APC as demonstrated by the ratio of cells exhibitinghigh versus low fluorescence intensity and by the magnitudeof the calcium signal in the activated population.Short-term interaction of T cells with less potent APC orwith efficient APC in the presence of low antigen concentrationresulted in decreased calcium signaling. CD28-mediated costimulation enhanced the magnitude and sustainedthe increase of intracellular calcium levels. In linewith the strong and sustained calcium signals, the activationof the calcium-dependent transcription factors NF-AT,AP-1, and NF-B was induced.Conclusions: Flow cytometric methods, feasible for therapid and flexible analysis of calcium signaling upon antigen-specificT-cell activation, were established. Kinetics ofthe increase of mean fluorescence intensity reflected thecalcium response of the total cell population whereasstatistical analysis of fluorescence intensity at selectedtime points provided information on the activation state ofsingle cells. Cytometry 47:207?216, 2002.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban T-cell activation antigen-presenting cell calcium signal costimulation
Megjelenés:	Cytometry. - 47 : 4 (2002), p. 207-216. -
További szerzők:	Detre, Cynthia Gogolák Péter (1968-) (biológus, immunológus) Kolonics Attila Magócsi Mária Rajnavölgyi Éva (1950-) (immunológus)
Pályázati támogatás:	030826 OTKA NKFP 0186/1999 Egyéb
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Saját polcon: