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1.

001-es BibID:BIBFORM071907
035-os BibID:(cikkazonosító)62 (WoS)000423384000001 (Scopus)85041107428
Első szerző:Agod Zsófia
Cím:Signaling Lymphocyte Activation Molecule Family 5 Enhances Autophagy and Fine-Tunes Cytokine Response in Monocyte-Derived Dendritic Cells via Stabilization of Interferon Regulatory Factor 8 / Zsofia Agod, Kitti Pazmandi, Dora Bencze, Gyorgy Vereb, Tamas Biro, Attila Szabo, Eva Rajnavolgyi, Attila Bacsi, Pablo Engel, Arpad Lanyi
Dátum:2018
ISSN:1664-3224
Megjegyzések:Signaling lymphocyte activation molecule family (SLAMF) receptors are essential regulators of innate and adaptive immune responses. The function of SLAMF5/CD84, a family member with almost ubiquitous expression within the hematopoietic lineage is poorly defined. In this paper we provide evidence that in human monocyte-derived dendritic cells (moDCs) SLAMF5 increases autophagy, a degradative pathway, which is highly active in dendritic cells (DCs) and plays a critical role in orchestration of the immune response. While investigating the underlying mechanism, we found that SLAMF5 inhibited proteolytic degradation of interferon regulatory factor 8 (IRF8) a master regulator of the autophagy process by a mechanism dependent on the E3 ubiquitin ligase tripartite motif-containing protein 21 (TRIM21). Furthermore, we demonstrate that SLAMF5 influences the ratio of CD1a+ cells in differentiating DCs and partakes in the regulation of IL?1?, IL?23 and IL?12 production in LPS/IFN??activated moDCs in a manner that is consistent with its effect on IRF8 stability. In summary, our experiments identified SLAMF5 as a novel cell surface receptor modulator of autophagy and revealed an unexpected link between the SLAMF and IRF8 signaling pathways, both implicated in multiple human pathologies.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
SLAMF5
Autophagy
Dendritic Cells
IRF8
TRIM21
IL?12p70
LPS/IFN?
Megjelenés:Frontiers in Immunology. - 9 (2018), p. 1-16. -
További szerzők:Pázmándi Kitti Linda (1984-) (molekuláris biológus, immunológus) Bencze Dóra (1992-) Vereb György (1965-) (biofizikus, orvos) Bíró Tamás (1968-) (élettanász) Szabó Attila (1981-) (molekuláris biológus, immunológus, filozófus) Rajnavölgyi Éva (1950-) (immunológus) Bácsi Attila (1967-) (immunológus) Engel, Pablo Lányi Árpád (1962-) (biológus, immunológus)
Pályázati támogatás:NKFIH K 81676
Egyéb
NKFIH K 109444
Egyéb
Romanian Ministry of Education, Executive Agency For Higher Education, Research, Development and Innovation Funding, PNCDI II, project no. 119/2014
Egyéb
GINOP-2.3.2-15-2016-00050
GINOP
COST Action BM1404 Mye-EUNITER
Egyéb
János Bolyai Research Scholarship from the Hungarian Academy of Sciences
Egyéb
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2.

001-es BibID:BIBFORM020146
Első szerző:Altorjay István (belgyógyász, gasztroenterológus, onkológus)
Cím:Anti-TNF-alpha antibody (infliximab) therapy supports the recovery of eNOS and VEGFR2 protein expression in endothelial cells / Istvan Altorjay, Zoltan Vereb, Zoltan Serfozo, Ildiko Bacskai, Robert Batori, Ferenc Erdodi, Miklos Udvardy, Sandor Sipka, Arpad Lanyi, Eva Rajnavolgyi, Karoly Palatka
Dátum:2011
Megjegyzések:The aim of this study is to investigate the effect of sera obtained from patients of Crohn's disease treated by anti-TNF-alpha antibody (infliximab) on the expression of endothelial nitric oxide synthase (eNOS) and vascular endothelial growth factor receptor-2 (VEGFR2) protein in human umbilical vein endothelial cells (HUVEC) cultured in vitro. HUVEC was cultured in the presence of sera derived from patients before and after treatment, or from healthy individuals. Effects of sera on the expression of eNOS and VEGFR2 were monitored by determination of mRNA and protein levels using real time quantitative PCR and Western blot analysis, respectively. The serum of Crohn's patients contained elevated levels of TNF-alpha (34 +/- 1.80 pg/mL), which resulted in a decrease in the protein level of eNOS in HUVEC with a simultaneous induction of VEGFR2. Infliximab treatment normalized the expression level of these proteins by decreasing TNF-alpha level, particularly in those cases when clinical healing was also recorded, and it also conferred restitution of the level of angiogenic cytokines. Results suggest that altered angiogenesis possibly contributes to the initiation and perpetuation of inflammatory processes in Inflammatory Bowel Disease (IBD). Endothelial dysfunction, a selective feature of Crohn's disease is beneficially affected by intravascular TNF-alpha neutralization.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Crohn's disease
eNOS
HUVEC
inflammatory bowel disease
infliximab
TNF-alpha
Vascular endothelial growth factor receptor-2
Megjelenés:International Journal of Immunopathology and Pharmacology 24 : 2 (2011), p. 323-335. -
További szerzők:Veréb Zoltán (1980-) (immunológus, mikrobiológus, molekuláris biológus) Serfőző Zoltán Bacskai Ildikó (1985-) (immunológus) Bátori Róbert Károly (1983-) (biológus, biotechnológus) Erdődi Ferenc (1953-) (biokémikus) Udvardy Miklós (1947-) (belgyógyász, haematológus) Sipka Sándor (1945-) (laboratóriumi szakorvos) Lányi Árpád (1962-) (biológus, immunológus) Rajnavölgyi Éva (1950-) (immunológus) Palatka Károly (1961-) (belgyógyász, gasztroenterológus)
Pályázati támogatás:0046/NA/2006-2/OP-9
Egyéb
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3.

001-es BibID:BIBFORM020155
Első szerző:Calpe, Silvia
Cím:Identification and characterization of two related murine genes, Eat2a and Eat2b, encoding single SH2-domain adapters / Silvia Calpe, Erika Erdős, Gongxian Liao, Ninghai Wang, Svend Rietdijk, Maria Simarro, Beata Scholtz, Jill Mooney, Chang Hoon Lee, Min Sun Shin, Éva Rajnavölgyi, John Schatzle, Herbert C. Morse III, Cox Terhorst, Arpad Lanyi
Dátum:2006
ISSN:0093-7711
Megjegyzések:Human EAT-2 (SH2D1B) and SLAM-associated protein (SAP) (SH2D1A) are single SH2-domain adapters, which bind to specific tyrosine residues in the cytoplasmic tail of six signaling lymphocytic activation molecule (SLAM) (SLAMF1)-related receptors. Here we report that, unlike in humans, the mouse and rat Eat2 genes are duplicated with an identical genomic organization. The coding regions of the mouse Eat2a and Eat2b genes share 91% identity at the nucleotide level and 84% at the protein level; similarly, segments of introns are highly conserved. Whereas expression of mouse Eat2a mRNA was detected in multiple tissues, Eat2b was only detectable in mouse natural killer cells, CD8(+) stop T cells, and ovaries, suggesting a very restricted tissue expression of the latter. Both the EAT-2A and EAT-2B coimmunoprecipitated with mouse SLAM in transfected cells and augmented tyrosine phosphorylation of the cytoplasmic tail of SLAM. Both EAT-2A and EAT-2B bind to the Src-like kinases Fyn, Hck, Lyn, Lck, and Fgr, as determined by a yeast two-hybrid assay. However, unlike SAP, the EAT-2 proteins bind to their kinase domains and not to the SH3 domain of these kinases. Taken together, the data suggest that both EAT-2A and EAT-2B are adapters that recruit Src kinases to SLAM family receptors using a mechanism that is distinct from that of SAP.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
adapter proteins
EAT-2
SLAM
Src kinases
Megjelenés:Immunogenetics 58 : 1 (2006), p. 15-25. -
További szerzők:Erdős Erika Liao, Gongxian Wang, Ninghai Rietdijk, Svend Simarro, Maria Scholtz Beáta (1967-) (biokémikus, molekuláris biológus) Mooney, Jill Lee, Chang Hoon Shin, Min Sun Rajnavölgyi Éva (1950-) (immunológus) Schatzle, John Morse, Herbert C. III Terhorst, Cox Lányi Árpád (1962-) (biológus, immunológus)
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4.

001-es BibID:BIBFORM014116
Első szerző:Cavalieri, Duccio
Cím:DC-ATLAS : a systems biology resource to dissect receptor specific signal transduction in dendritic cells / Cavalieri Duccio, Rivero Damariz, Beltrame Luca, Buschow Sonja I., Calura Enrica, Rizzetto Lisa, Gessani Sandra, Gauzzi Maria C., Reith Walter, Baur Andreas, Bonaiuti Roberto, Brandizi Marco, De Filippo Carlotta, D'Oro Ugo, Draghici Sorin, Dunand-Sauthier Isabelle, Gatti Evelina, Granucci Francesca, Gündel Michaela, Kramer Matthijs, Kuka Mirela, Lanyi Arpad, Melief Cornelis J. M., van Montfoort Nadine, Ostuni Renato, Pierre Philippe, Popovici Razvan, Rajnavolgyi Eva, Schierer Stephan, Schuler Gerold, Soumelis Vassili, Splendiani Andrea, Stefanini Irene, Torcia Maria G., Zanoni Ivan, Zollinger Raphael, Figdor Carl G., Austyn Jonathan M.
Dátum:2010
ISSN:1745-7580
Megjegyzések:The advent of Systems Biology has been accompanied by the blooming of pathway databases. Currently pathways are defined generically with respect to the organ or cell type where a reaction takes place. The cell type specificity of the reactions is the foundation of immunological research, and capturing this specificity is of paramount importance when using pathway-based analyses to decipher complex immunological datasets. Here, we present DC-ATLAS, a novel and versatile resource for the interpretation of high-throughput data generated perturbing the signaling network of dendritic cells (DCs).RESULTS: Pathways are annotated using a novel data model, the Biological Connection Markup Language (BCML), a SBGN-compliant data format developed to store the large amount of information collected. The application of DC-ATLAS to pathway-based analysis of the transcriptional program of DCs stimulated with agonists of the toll-like receptor family allows an integrated description of the flow of information from the cellular sensors to the functional outcome, capturing the temporal series of activation events by grouping sets of reactions that occur at different time points in well-defined functional modules.CONCLUSIONS: The initiative significantly improves our understanding of DC biology and regulatory networks. Developing a systems biology approach for immune system holds the promise of translating knowledge on the immune system into more successful immunotherapy strategies.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Immunome Research. - 6 : 10 (2010), p. 1-12. -
További szerzők:Rivero, Damariz Beltrame, Luca Buschow, Sonja I. Calura, Enrica Rizzetto, Lisa Gessani, Sandra Gauzzi, Maria C. Reith, Walter Baur, Andreas Bonaiuti, Roberto Brandizi, Marco De Filippo, Carlotta D'Oro, Ugo Draghici, Sorin Dunand-Sauthier, Isabelle Gatti, Evelina Granucci, Francesca Gündel, Michaela Kramer, Matthijs Kuka, Mirela Lányi Árpád (1962-) (biológus, immunológus) Melief, Cornelis J. M. van Montfoort, Nadine Ostuni, Renato Pierre, Philippe Popovici, Razvan Rajnavölgyi Éva (1950-) (immunológus) Schierer, Stephan Schuler, Gerold Soumelis, Vassili Splendiani, Andrea Stefanini, Irene Torcia, Maria G. Zanoni, Ivan Zollinger, Raphael Figdor, Carl G. Austyn, Jonathan M.
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5.

001-es BibID:BIBFORM032051
Első szerző:Fekete Tünde (immunológus, molekuláris biológus, mikrobiológus)
Cím:Constraints for monocyte-derived dendritic cell functions under inflammatory conditions / Fekete Tünde, Szabo Attila, Beltrame Luca, Vivar Nancy, Pivarcsi Andor, Lanyi Arpad, Cavalieri Duccio, Rajnavölgyi Eva, Rethi Bence
Dátum:2012
ISSN:0014-2980
Megjegyzések:The activation of TLRs expressed by macrophages or DCs, in the long run, leads to persistently impaired functionality. TLR signals activate a wide range of negative feedback mechanisms; it is not known, however, which of these can lead to long-lasting tolerance for further stimulatory signals. In addition, it is not yet understood how the functionality of monocyte-derived DCs (MoDCs) is influenced in inflamed tissues by the continuous presence of stimulatory signals during their differentiation. Here we studied the role of a wide range of DC-inhibitory mechanisms in a simple and robust model of MoDC inactivation induced by early TLR signals during differentiation. We show that the activation-induced suppressor of cytokine signaling 1 (SOCS1), IL-10, STAT3, miR146a and CD150 (SLAM) molecules possessed short-term inhibitory effects on cytokine production but did not induce persistent DC inactivation. On the contrary, the LPS-induced IRAK-1 downregulation could alone lead to persistent MoDC inactivation. Studying cellular functions in line with the activation-induced negative feedback mechanisms, we show that early activation of developing MoDCs allowed only a transient cytokine production that was followed by the downregulation of effector functions and the preservation of a tissue-resident non-migratory phenotype.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
DC
Endotoxin tolerance
IRAK-1
TLR
Megjelenés:European Journal of Immunology 42 : 2 (2012), p. 458-469. -
További szerzők:Szabó Attila (1981-) (molekuláris biológus, immunológus, filozófus) Beltrame, Luca Vivar, Nancy Pivarcsi Andor Lányi Árpád (1962-) (biológus, immunológus) Cavalieri, Duccio Rajnavölgyi Éva (1950-) (immunológus) Réthi Bence (1973-) (biológus, immunológus)
Pályázati támogatás:TORNADO 222720 (felhívás kód: FP7-KBBE-2007-2A)
FP7
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6.

001-es BibID:BIBFORM001482
Első szerző:Gogolák Péter (biológus, immunológus)
Cím:Differentiation of CD1a- and CD1a+ monocyte-derived dendritic cells is biased by lipid environment and PPARgamma / Gogolak P., Réthi B., Szatmári I., Nagy L., Lányi Á., Dezső B., Rajnavölgyi É.
Dátum:2007
Megjegyzések:Accumulating data have shown that the microenvironment of dendritic cells modulates subtype differentiation and CD1 expression, but the mechanisms by which exogenous factors confer these effects are poorly understood. Here we describe the dependence of CD1a- monocyte-derived dendritic cell (moDC) development on lipids associated with the expression of peroxisome proliferator-activated receptor-gamma (PPARgamma). We also show the consecutive differentiation of immature CD1a-PPARgamma+ moDCs to CD1a+PPARgamma- cells limited by serum lipoproteins and terminated by proinflammatory cytokines. Immature CD1a- moDCs possess higher internalizing capacity than CD1a+ cells, whereas both activated subtypes have similar migratory potential but differ in their cytokine and chemokine profiles, which translates to distinct T-lymphocyte-polarizing capacities. CD1a+ moDCs stand out by their capability to secrete high amounts of IL-12p70 and CCL1. As lipoproteins skew moDC differentiation toward the generation of CD1a-PPARgamma+ cells and inhibit the development of CD1a+PPARgamma- cells, we suggest that the uptake of lipids results in endogenous PPARgamma agonists that induce a cascade of gene transcription coordinating lipid metabolism, the expression of lipid-presenting CD1 molecules, subtype dichotomy, and function. The presence of CD1a-PPARgamma+ and CD1a+PPARgamma- DCs in lymph nodes and in pulmonary Langerhans cell histiocytosis confirms the functional relevance of these DC subsets in vivo.
Tárgyszavak:Orvostudományok Természettudományok Elméleti orvostudományok Biológiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban
dendritic cell
differentiation
CD1a
PPARgamma
lipid
lipoprotein
T cell polarization
Megjelenés:Blood. - 109 : 2 (2007), p. 643-652. -
További szerzők:Réthi Bence (1973-) (biológus, immunológus) Lányi Árpád (1962-) (biológus, immunológus) Dezső Balázs (1951-) (pathológus) Rajnavölgyi Éva (1950-) (immunológus) Szatmári István (1971-) (biológus) Nagy László (1966-) (molekuláris sejtbiológus, biokémikus)
Internet cím:elektronikus változat
elektronikus változat
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7.

001-es BibID:BIBFORM028890
Első szerző:Lányi Árpád (biológus, immunológus)
Cím:The homolog of the five SH3-domain protein (HOFI/SH3PXD2B) regulates lamellipodia formation and cell spreading / Lányi Á., Baráth M., Péterfi Z., Bogel G., Orient A., Simon T., Petrovszki E., Kis-Tóth K., Sirokmány G., Rajnavölgyi É., Terhorst C., Buday L., Geiszt M.
Dátum:2011
ISSN:1932-6203
Megjegyzések:Motility of normal and transformed cells within and across tissues requires specialized subcellular structures, e. g. membrane ruffles, lamellipodia and podosomes, which are generated by dynamic rearrangements of the actin cytoskeleton. Because the formation of these sub-cellular structures is complex and relatively poorly understood, we evaluated the role of the adapter protein SH3PXD2B [HOFI, fad49, Tks4], which plays a role in the development of the eye, skeleton and adipose tissue. Surprisingly, we find that SH3PXD2B is requisite for the development of EGF-induced membrane ruffles and lamellipodia, as well as for efficient cellular attachment and spreading of HeLa cells. Furthermore, SH3PXD2B is present in a complex with the non-receptor protein tyrosine kinase Src, phosphorylated by Src, which is consistent with SH3PXD2B accumulating in Src-induced podosomes. Furthermore, SH3PXD2B closely follows the subcellular relocalization of cortactin to Src-induced podosomes, EGF-induced membrane ruffles and lamellipodia. Because SH3PXD2B also forms a complex with the C-terminal region of cortactin, we propose that SH3PXD2B is a scaffold protein that plays a key role in regulating the actin cytoskeleton via Src and cortactin.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
lamellipodia, podosome
scaffold protein
Megjelenés:PLoS One. - 6 : 8 (2011), p. e23653. -
További szerzők:Baráth Mónika (1980-) (Phd hallgató) Péterfi Zalán Bogel Gábor Orient Anna Simon Tünde (1984-) (biokémikus, molekuláris biológus) Petrovszki Enikő Kis-Tóth Katalin (1975-) (immunológus) Sirokmány Gábor Rajnavölgyi Éva (1950-) (immunológus) Terhorst, Cox Buday László Geiszt Miklós
Pályázati támogatás:TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
Molekuláris immunológia
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8.

001-es BibID:BIBFORM060944
Első szerző:Pázmándi Kitti Linda (molekuláris biológus, immunológus)
Cím:Oxidative modification enhances the immunostimulatory effects of extracellular mitochondrial DNA / K. Pázmándi, Zs. Agod, B. V. Kumar, A. Szabó, T. Fekete, V. Sógor, A. Veres, I. Boldogh, E. Rajnavölgyi, A. Lányi, A. Bácsi
Dátum:2015
Tárgyszavak:Orvostudományok Elméleti orvostudományok idézhető absztrakt
Megjelenés:European Journal of Clinical Investigation. - 45 : 2 (2015), p. 65. -
További szerzők:Agod Zsófia Kumar, Brahma V. Szabó Attila (1981-) (molekuláris biológus, immunológus, filozófus) Fekete Tünde (1984-) (immunológus, molekuláris biológus, mikrobiológus) Somogyi Viktória (1989-) (biotechnológus) Veres Ágota (laboráns) Boldogh István Rajnavölgyi Éva (1950-) (immunológus) Lányi Árpád (1962-) (biológus, immunológus) Bácsi Attila (1967-) (immunológus)
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9.

001-es BibID:BIBFORM055879
Első szerző:Pázmándi Kitti Linda (molekuláris biológus, immunológus)
Cím:Reactive oxygen species generated by NAD(P)H oxidases in ragweed subpollen particles activate human dendritic cells / Pázmándi Kitti, Kumar Brahma V., Szabó Krisztina, Boldogh István, Szöőr Árpád, Vereb György, Veres Ágota, Lányi Árpád, Rajnavölgyi Éva, Bácsi Attila
Dátum:2012
Tárgyszavak:Természettudományok Biológiai tudományok idézhető absztrakt
Megjelenés:Immunology 137 (2012), p. 458. -
További szerzők:Kumar, Brahma V. Szabó Krisztina (1987-) (Molekuláris biológus) Boldogh István Szöőr Árpád (1984-) (orvos) Vereb György (1965-) (absztraktok, könyvfejezetek) Veres Ágota (laboráns) Lányi Árpád (1962-) (biológus, immunológus) Rajnavölgyi Éva (1950-) (immunológus) Bácsi Attila (1967-) (immunológus)
Borító:

10.

001-es BibID:BIBFORM055554
Első szerző:Pázmándi Kitti Linda (molekuláris biológus, immunológus)
Cím:Oxidative modification enhances the immunostimulatory effects of extracellular mitochondrial DNA on plasmacytoid dendritic cells / Kitti Pazmandi, Zsofia Agod, Brahma V. Kumar, Attila Szabo, Tunde Fekete, Viktoria Sogor, Agota Veres, Istvan Boldogh, Eva Rajnavolgyi, Arpad Lanyi, Attila Bacsi
Dátum:2014
ISSN:0891-5849
Megjegyzések:Inflammation is associated with oxidative stress and characterized by elevated levels of damage-associated molecular pattern (DAMP) molecules released from injured or even living cells into the surrounding microenvironment. One of these endogenous danger signals is the extracellular mitochondrial DNA (mtDNA) containing evolutionary conserved unmethylated CpG repeats. Increased levels of reactive oxygen species (ROS) generated by recruited inflammatory cells modify mtDNA oxidatively resulting primarily in accumulation of 8-oxo-7,8-dihydroguanine (8-oxoG) lesions. In this study, we examined the impact of native and oxidatively modified mtDNAs on the phenotypic and functional properties of plasmacytoid dendritic cells (pDCs), which possess a fundamental role in the regulation of inflammation and T cell immunity. Treatment of human primary pDCs with native mtDNA up-regulated the expression of a co-stimulatory molecule (CD86), a specific maturation marker (CD83), and a main antigen-presenting molecule (HLA-DQ) on the cell surface, as well as increased TNF-? and IL-8 production from the cells. These effects were more apparent when pDCs were exposed to oxidatively modified mtDNA. Neither native nor oxidized mtDNA molecules were able to induce interferon (IFN)-? secretion from pDCs unless they formed a complex with human cathelicidin LL-37, an antimicrobial peptide. Interestingly, simultaneous administration of a Toll-like receptor (TLR)9 antagonist abrogated the effects of both native and oxidized mtDNAs on human pDCs. In a murine model, oxidized mtDNA also proved a more potent activator of pDCs compared to the native form, except for induction of IFN-? production. Collectively, we demonstrate here for the first time that elevated levels of 8-oxoG bases in the extracellular mtDNA induced by oxidative stress increase the immunostimulatory capacity of mtDNA on pDCs.
Tárgyszavak:Természettudományok Biológiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Plasmacytoid dendritic cells
Extracellular mitochondrial DNA
Oxidative stress
8-oxoguanine base
Inflammation
Megjelenés:Free Radical Biology and Medicine. - 77 (2014), p. 281-290. -
További szerzők:Agod Zsófia Kumar, Brahma V. Szabó Attila (1981-) (molekuláris biológus, immunológus, filozófus) Fekete Tünde (1984-) (immunológus, molekuláris biológus, mikrobiológus) Somogyi Viktória (1989-) (biotechnológus) Veres Ágota (laboráns) Boldogh István Rajnavölgyi Éva (1950-) (immunológus) Lányi Árpád (1962-) (biológus, immunológus) Bácsi Attila (1967-) (immunológus)
Pályázati támogatás:K-109595
OTKA
TAMOP-4.2.2.A-11/1/KONV-2012-0023
TÁMOP
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11.

001-es BibID:BIBFORM041944
Első szerző:Pázmándi Kitti Linda (molekuláris biológus, immunológus)
Cím:Ragweed subpollen particles of respirable size activate human dendritic cells / Pazmandi K., Kumar B. V., Szabo K., Boldogh I., Szoor A., Vereb G., Veres A., Lanyi A., Rajnavolgyi E., Bacsi A.
Dátum:2012
ISSN:1932-6203
Megjegyzések:Ragweed (Ambrosia artemisiifolia) pollen grains, which are generally considered too large to reach the lower respiratory tract, release subpollen particles (SPPs) of respirable size upon hydration. These SPPs contain allergenic proteins and functional NAD(P)H oxidases. In this study, we examined whether exposure to SPPs initiates the activation of human monocyte-derived dendritic cells (moDCs). We found that treatment with freshly isolated ragweed SPPs increased the intracellular levels of reactive oxygen species (ROS) in moDCs. Phagocytosis of SPPs by moDCs, as demonstrated by confocal laser-scanning microscopy, led to an up-regulation of the cell surface expression of CD40, CD80, CD86, and HLA-DQ and an increase in the production of IL-6, TNF-?, IL-8, and IL-10. Furthermore, SPP-treated moDCs had an increased capacity to stimulate the proliferation of naïve T cells. Co-culture of SPP-treated moDCs with allogeneic CD3(+) pan-T cells resulted in increased secretion of IFN-? and IL-17 by T cells of both allergic and non-allergic subjects, but induced the production of IL-4 exclusively from the T cells of allergic individuals. Addition of exogenous NADPH further increased, while heat-inactivation or pre-treatment with diphenyleneiodonium (DPI), an inhibitor of NADPH oxidases, strongly diminished, the ability of SPPs to induce phenotypic and functional changes in moDCs, indicating that these processes were mediated, at least partly, by the intrinsic NAD(P)H oxidase activity of SPPs. Collectively, our data suggest that inhaled ragweed SPPs are fully capable of activating dendritic cells (DCs) in the airways and SPPs' NAD(P)H oxidase activity is involved in initiation of adaptive immune responses against innocuous pollen proteins.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Doktori iskola
Molekuláris Medicina
Open Access
Megjelenés:Plos One. - 7 : 12 (2012), p. e52085. -
További szerzők:Kumar, Brahma V. Szabó Krisztina (1987-) (Molekuláris biológus) Boldogh István Szöőr Árpád (1984-) (orvos) Vereb György (1965-) (biofizikus, orvos) Veres Ágota (laboráns) Lányi Árpád (1962-) (biológus, immunológus) Rajnavölgyi Éva (1950-) (immunológus) Bácsi Attila (1967-) (immunológus)
Pályázati támogatás:TÁMOP-4.2.2/B-10/1-2010-0024
TÁMOP
Molekuláris Sejt- és Immunbiológiai Doktori Iskola
TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
Az oxidatív DNS károsodások javítása és a gyulladás kialakulásának kapcsolata
TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
Jelátviteli kapcsolatok ős- és dendritikus sejt altípusokban
Bolyai János Ösztöndíj
MTA
DE OEC Bridging Fund
Egyéb
K 73347
OTKA
NK 101538
OTKA
Internet cím:DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

12.

001-es BibID:BIBFORM014046
Első szerző:Petheő Gábor L.
Cím:Molecular and Functional Characterization of H(v)1 Proton Channel in Human Granulocytes / Petheo Gabor L., Anna Orient, Monika Barath, Istvan Kovacs, Bence Rethi, Arpad Lanyi, Aniko Rajki, Eva Rajnavolgyi, Miklos Geiszt
Dátum:2010
Megjegyzések:Voltage-gated proton current (I-Hv) has been characterized in several cell types, but the majority of the data was collected in phagocytes, especially in human granulocytes. The prevailing view about the role of I-Hv in phagocytes is that it is an essential supporter of the intense and sustained activity of Nox2 (the core enzyme of the phagocyte NADPH oxidase complex) during respiratory burst. Recently H(v)1, a voltage-gated proton channel, was cloned, and leukocytes from H(v)1 knockout mice display impaired respiratory burst. On the other hand, hardly anything is known about H(v)1 in human granulocytes. Using qPCR and a self made antibody, we detected a significant amount of H(v)1 in human eosinophil and neutrophil granulocytes and in PLB-985 leukemia cells. Using different crosslinking agents and detergents in reducing and non-reducing PAGE, significant expression of H(v)1 homodimers, but not that of higher-order multimers, could be detected in granulocytes. Results of subcellular fractionation and confocal imaging indicate that H(v)1 is resident in both plasmalemmal and granular membrane compartments of resting neutrophils. Furthermore, it is also demonstrated that H(v)1 accumulates in phagosome wall during zymosan engulfment together with, but independently of Nox2. During granulocytic differentiation early and parallel upregulation of H(v)1 and Nox2 expression was observed in PLB-985 cells. The upregulation of H(v)1 or Nox2 expression did not require the normal expression of the other molecule. Using RNA interference, we obtained strong correlation between H(v)1 expression and I-Hv density in PLB-985 cells. It is also demonstrated that a massive reduction in H(v)1 expression can limit the Nox2 mediated superoxide production of PLB-985 granulocytes. In summary, beside monomers native H(v)1 forms stable proton channel dimer in resting and activated human granulocytes. The expression pattern of H(v)1 in granulocytes is optimized to support intense NADPH oxidase activity.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Chronic Granulomatous-Disease
Phagocyte Respiratory Burst
Human-Neutrophilis
Superoxide-Production
Reactive Oxygen
Voltage Sensor
2 Pores
HV1
Conductance
Currents
Megjelenés:PloS One. - 5 : 11 (2010), p. e14081. -
További szerzők:Orient Anna Baráth Mónika (1980-) (Phd hallgató) Kovács István (Budapest) Réthi Bence (1973-) (biológus, immunológus) Lányi Árpád (1962-) (biológus, immunológus) Rajki Anikó Rajnavölgyi Éva (1950-) (immunológus) Geiszt Miklós
Pályázati támogatás:K 63700
OTKA
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:
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