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001-es BibID:	BIBFORM065606
Első szerző:	Fekete Tünde (immunológus, molekuláris biológus, mikrobiológus)
Cím:	Interferon gamma boosts the nucleotide oligomerization domain 2-mediated signaling pathway in human dendritic cells in an X-linked inhibitor of apoptosis protein and mammalian target of rapamycin-dependent manner / Tünde Fekete, Gabor Koncz, Brigitta Szabo, Andrea Gregus, Eva Rajnavölgyi
Dátum:	2017
ISSN:	1672-7681 2042-0226
Megjegyzések:	The cytoplasmic nucleotide oligomerization domain 2 (NOD2) receptor recognizes the bacterial cell wall componentmuramyl dipeptide (MDP). NOD2 ligation initiates the nuclear factor kappa B and the mitogen-activated protein kinasecascades. However, administering MDP alone is insufficient to elicit strong cytokine responses in various immune cells,including dendritic cells (DCs). Because the simultaneous presence of various microbial products and cytokines ininflamed tissues modulates DC function, we initiated this study to examine how interferon gamma (IFNc), a centralmodulator of inflammation, affects the NOD2-mediated signaling pathway in human conventional DCs (cDCs).Synergistic stimulation of DCs with MDP and IFNc increased the expression of CD40, CD80, CD83, CD86, and humanleukocyte antigen DQ proteins and significantly elevated the production of pro-inflammatory cytokines IL-1b, IL-6, IL-12,and tumour necrosis factor (TNF), as well as anti-inflammatory cytokine IL-10. Furthermore, the simultaneous presenceofMDP and IFNc was necessary to decrease IkBa protein levels. By investigating various mechanisms implicated in MDPandIFNc-mediated signaling pathways, we revealed that the increased production of pro-inflammatory cytokines ishighly dependent on the X-linked inhibitor of apoptosis protein (XIAP) but not on cellular IAP1 and IAP2. We also foundthat the NOD2 signaling pathway is regulated by the mammalian target of rapamycin (mTOR) but is not affected byphosphatidylinositol-3 kinase or signal transducer and activator of transcription 1 inhibition. Our results demonstrate, forthe first time, that IFNc positively affects NOD2-mediated signaling in human cDCs, in a manner considerably dependenton XIAP and partially dependent on mTOR.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban dendritic cell mTOR NOD2 XIAP
Megjelenés:	Cellular And Molecular Immunology 14 : 4 (2017), p. 380-391. -
További szerzők:	Koncz Gábor (1970-) (biológus, immunológus) Szabó Brigitta Gregus Andrea (1980-) (biológus) Rajnavölgyi Éva (1950-) (immunológus)
Pályázati támogatás:	NN114423 OTKA
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM005575
Első szerző:	Jiao, Hong
Cím:	Novel and recurrent STAT3 mutations in hyper-IgE syndrome patients from different ethnic groups / Hong Jiao, Beata Toth, Melinda Erdos, Ingegerd Fransson, Eva Rakoczi, Istvan Balogh, Zoltan Magyarics, Beata Derfalvy, Gabriella Csorba, Anna Szaflarska, Andre Megarbane, Carlo Akatcherian, Ghassan Dbaibo, Eva Rajnavolgyi, Lennart Hammarstrom, Juha Kere, Gerard Lefranc, Laszlo Marodi
Dátum:	2008
Megjegyzések:	We Performed clinical, immunological and genetic studies of 12 hyper-IgE syndrome (HIES) patients from 4 Hungarian, 2 Lebanese, one Russian, one Polish, and one Swedish families with autosomal dominant (AD) or sporadic forms of the disease to reveal cross-ethnicity of recurrent and novel mutations in the signal transducer and activator of transcription-3 gene (STAT3). Four patients from 3 Hungarian families, and one Russian, and one Swedish patient carried the heterozygous R382W germline mutation at the DNA-binding site of STAT3. The recurrent V637M mutation affecting the SRC homology 2 (SH2) domain was detected in one Lebanese and one Polish family, and the V463del deletion located in the DNA-binding domain was unveiled in another Lebanese family. A novel H332Y mutation affecting the DNA-binding site of STAT3 in three Hungarian patients from a Gypsy family was also found. The segregation of this mutation with HIES, restriction fragment length polymorphism analysis of STAT3 from patients and controls and the negligible production upon IL-6 stimulation of monocyte chemotactic protein-1 by the patient's blood mononuclear cells suggested that the H332Y mutation was disease-causing. These data suggest, that dominant negative mutations of the DNA-binding and SH2 domains of STAT3 cause AD and sporadic cases of HIES in different ethnic groups with R382W as the predominant mutation found in 5 of the 9 families. Functional and genetic data support that the novel H332Y mutation may result in the loss of function of STAT3 and leads to the HIES phenotype.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Hyper-IgE syndrome STAT3 mutation DNA Cells egyetemen (Magyarországon) készült közlemény
Megjelenés:	Molecular Immunology. - 46 : 1 (2008), p. 202-206. -
További szerzők:	Lajszné Tóth Beáta (1978-) (molekuláris biológus) Erdős Melinda (1975-) (infektológus, gyermekimmunológus) Fransson, Ingegerd Rákóczi Éva (1962-) (klinikai szakorvos) Balogh István (1972-) (molekuláris biológus, genetikus) Magyarics Zoltán (1982-) (immunológus) Dérfalvy Beáta Csorba Gabriella Éva (1978-) (gyermekgyógyász) Szaflarska, Anna Megarbane, Andre Akatcherian, Carlo Dbaibo, Ghassan Rajnavölgyi Éva (1950-) (immunológus) Hammarström, Lennart Kere, Juha Lefranc, Gerard Maródi László (1949-) (gyermekgyógyász infektológus, immunológus)
Internet cím:	elektronikus változat DOI elektronikus változat
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001-es BibID:	BIBFORM065583
Első szerző:	Simon Ágnes (laboratóriumi szakorvos)
Cím:	Modeling MHC class II molecules and their bound peptides as expressed at the cell surface / Á. Simon, I. Simon, É. Rajnavölgyi
Dátum:	2002
ISSN:	0161-5890
Megjegyzések:	A detailed insight to the structure of a given major histocompatibility complex (MHC)-peptide complex can strongly support and also improve the analysis of the peptide binding capabilities of the MHC molecule and the characterization of the developing T cell response. The number of MHC class II-peptide crystal structures is limited, therefore constructing and analyzing computer models can serve as efficient complementary tools when someone deals with experimentally determined binding and/or functional data. Commercial programs are available for modeling protein and protein-protein complexes, in general. However, more accurate results can be obtained if the parameters are directly optimized to a given complex, especially in the case of special proteins as MHC class II, an integral membrane protein, whose functional parts behave like regular globular proteins. Here, we present the optimization of an approach used for modeling MHC class II molecules complexed with various peptides fitting into the binding groove and several ways to analyze them with the help of experimental data.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban MHC class II Molecular modeling Energy minimization MHC-peptide complex
Megjelenés:	Molecular Immunology. - 38 : 9 (2002), p. 681-687. -
További szerzők:	Simon István Rajnavölgyi Éva (1950-) (immunológus)
Pályázati támogatás:	T30566 OTKA T34131 OTKA T 30826 OTKA NKFP 0186/1999 Egyéb
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM052647
Első szerző:	Szabó Attila (molekuláris biológus, immunológus, filozófus)
Cím:	Finding a fairy in the forest : ELF4, a novel and critical element of type I interferon responses / Attila Szabo, Éva Rajnavolgyi
Dátum:	2014
ISSN:	1672-7681 2042-0226
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban innate immunity interferon Pattern recognition receptors
Megjelenés:	Cellular and Molecular Immunology. - 11 : 3 (2014), p. 218-220. -
További szerzők:	Rajnavölgyi Éva (1950-) (immunológus)
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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