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001-es BibID:	BIBFORM065577
Első szerző:	Gogolák Péter (biológus, immunológus)
Cím:	Mapping of a Protective Helper T Cell Epitope of Human Influenza A Virus Hemagglutinin / Péter Gogolák, Ágnes Simon, Attila Horváth, Bence Réthi, István Simon, Katalin Berkics, Éva Rajnavölgyi, Gábor K. Tóth
Dátum:	2000
ISSN:	0006-291X
Megjegyzések:	The synthetic peptide comprising the 317-341 region of human influenza A virus (H1N1 subtype) hemagglutinin elicits peptide-specific antibody and helper T cell responses and confers protection against lethal virus infection. Molecular mapping of the 317-329 region, which encompasses the epitope recognized by peptide-specific T cells, revealed that the minimal size required for T cell activation was the 317-326 segment. The most likely peptide alignment, which placed 320Leu to pocket 1 of the I-E(d) peptide binding groove, was predicted by molecular mechanics calculations performed with the parental and with the Ala-substituted analogs. In line with the prediction data, the results of the peptide binding assay, where the relative binding efficiency to I-E(d) molecules expressed on the surface of antigen-presenting cells was monitored, identified the 320-326 core sequence interacting with the major histocompatibility class II peptide binding groove. Functional analysis of Ala-substituted variants by functional assays and by calculating the surface-accessible areas of the single peptidic amino acids in the I-E(d)-peptide complexes demonstrated that 324Pro is a primary contact residue for the T cell receptor. Our results show that this type of analysis offers a suitable tool for molecular mapping of helper T cell epitopes and thus provides valuable data for subunit vaccine design.Copyright 2000 Academic Press.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Biochemical And Biophysical Research Communications 270 : 1 (2000), p. 190-198. -
További szerzők:	Simon Ágnes (1969-) (laboratóriumi szakorvos) Horváth Attila (orvos) Réthi Bence (1973-) (biológus, immunológus) Simon István Berkics Katalin Rajnavölgyi Éva (1950-) (immunológus) Tóth Gábor K.
Pályázati támogatás:	T022540 OTKA T030826 OTKA T030566 OTKA FKFP 0186/1999 Egyéb AKP 98-13 3,3 Egyéb
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM065582
Első szerző:	Horváth Attila (orvos)
Cím:	Serum amyloid P component inhibits influenza A virus infections : in vitro and in vivo studies / A. Horváth, I. Andersen, K. Junker, B. Lyck Fogh-Schultz, E. Holm Nielsen, S. Gizurarson, O. Andersen, J. Kármán, E. Rajnavölgyi, A. Erdei, S.-E. Svehag
Dátum:	2001
ISSN:	0166-3542
Megjegyzések:	Serum amyloid P component (SAP) binds in vitro Ca(2+)-dependently to several ligands including oligosaccharides with terminal mannose and galactose. We have earlier reported that SAP binds to human influenza A virus strains, inhibiting hemagglutinin (HA) activity and virus infectivity in vitro. These studies were extended to comprise five mouse-adapted influenza A strains, two swine influenza A strains, a mink influenza A virus, a ferret influenza A reassortant virus, a influenza B virus and a parainfluenza 3 virus. The HA activity of all these viruses was inhibited by SAP. Western blotting showed that SAP bound to HA trimers, monomers and HA1 and HA2 subunits of influenza A virus. Binding studies indicated that galactose, mannose and fucose moieties contributed to the SAP reacting site(s). Intranasal administration of human SAP to mice induced no demonstrable toxic reactions, and circulating antibodies against SAP were not detected. Preincubation of virus (A/Japan/57) with SAP prevented primary infection of mice and development of antiviral antibodies. After a single intranasal administration of SAP (40 microg) 1 h before primary infection with virus (2LD(50)), nine out of 10 mice survived on day 10 and these mice approached normal body weight, whereas control mice (one out of five surviving on day 10) died. The data provide evidence of the potential of intranasally administered SAP for prophylactic treatment of influenza A virus infections in humans.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Antiviral effect Serum amyloid P component Influenza A virus
Megjelenés:	Antiviral Research 52 : 1 (2001), p. 43-53. -
További szerzők:	Andersen, Inger Junker, Kirsten Lyck Fogh-Schultz, B. Holm Nielsen, Ellen Gizurarson, Sveinbjörn Andersen, Ove Kármán József Rajnavölgyi Éva (1950-) (immunológus) Erdei Anna Svehag, Sven Erik
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM065576
Első szerző:	Igaz Péter
Cím:	Soluble interleukin-6 receptor (sIL-6R) makes IL-6R negative T cell line respond to IL-6 : it inhibits TNF production / Peter Igaz, Attila Horváth, Barbara Horváth, Csaba Szalai, Éva Pállinger, Éva Rajnavölgyi, Sara Tóth, Stefan Rose-John, András Falus
Dátum:	2000
ISSN:	0165-2478
Megjegyzések:	The receptor for interleukin-6 (IL-6) consists of two subunits: a ligand specific IL-6Ralpha and gp130 that is responsible for signal-transduction. A soluble form of the ligand specific chain was described that when complexed to IL-6 is capable of binding to the membrane-bound gp130 subunit and thus can elicit signal-transduction. This soluble receptor can act on cells that express only the gp130 but not the ligand-specific subunit of the IL-6R. This phenomenon, called trans-signaling, introduced a novel aspect of cytokine action. In this study we examined the response of Jurkat cells, that are known not to express IL-6Ralpha, to IL-6, the soluble IL-6 receptor (sIL-6R) and a covalent complex of IL-6 and sIL-6R termed Hyper-IL-6. We studied the expression of tumour necrosis factor (TNF) and interferon-gamma (IFN-gamma). The complex of IL-6+sIL-6R and Hyper-IL-6 inhibited significantly the production of TNF in a gp130-dependent manner, whereas no differences in IFN-gamma expression were found. IL-6 and sIL-6R alone were not effective. Because we did not detect major differences in the TNF mRNA levels upon treatments, we conclude that the inhibition of TNF production should occur at the post-transcriptional level. These results provide another example of trans-signaling and underline the physiological importance of sIL-6R, and in the case of Hyper-IL-6 its possible therapeutic application can also be considered.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Soluble IL-6 receptor Hyper-IL-6 Jurkat cells Tumour necrosis factor Interferon-gamma
Megjelenés:	Immunology Letters 71 : 3 (2000), p. 143-148. -
További szerzők:	Horváth Attila (orvos) Horváth Barbara Szalai Csaba Pállinger Éva Rajnavölgyi Éva (1950-) (immunológus) Tóth Sára Rose-John, Stefan Falus András
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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