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1.

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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2.

001-es BibID:BIBFORM002005
Első szerző:Fluur, Caroline
Cím:Potential role for IL-7 in Fas-mediated T cell apoptosis during HIV infection / Caroline Fluur, Angelo De Milito, Terry J. Fry, Nancy Vivar, Liv Eidsmo, Ann Atlas, Cristina Federici, Paola Matarrese, Mariantonia Logozzi, Éva Rajnavölgyi, Crystal L. Mackall, Stefano Fais, Francesca Chiodi, and Bence Réthi
Dátum:2007
Megjegyzések:IL-7 promotes survival of resting T lymphocytes and induces T cell proliferation in lymphopenic conditions. As elevated IL-7 levels occur in HIV-infected individuals in addition to high Fas expression on T cells and increased sensitivity to Fas-induced apoptosis, we analyzed whether IL-7 has a regulatory role in Fas-mediated T cell apoptosis. We show that IL-7 up-regulates Fas expression on naive and memory T cells through a mechanism that involves translocation of Fas molecules from intracellular compartments to the cell membrane. IL-7 induced the association of Fas with the cytoskeletal component ezrin and a polarized Fas expression on the cell surface. The potential role of IL-7 in Fas up-regulation in vivo was verified in IL-7-treated macaques and in HIV-infected or chemotherapy treated patients by the correlation between serum IL-7 levels and Fas expression on T cells. IL-7 treatment primed T cells for Fas-induced apoptosis in vitro and serum IL-7 levels correlated with the sensitivity of T cells to Fas-induced apoptosis in HIV-infected individuals. Our data suggest an important role for IL-7 in Fas-mediated regulation of T cell homeostasis. Elevated IL-7 levels associated with lymphopenic conditions, including HIV-infection, might participate in the increased sensitivity of T cells for activation-induced apoptosis
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
IL-7
Fas
HIV
Megjelenés:Journal of Immunology. - 178 : 8 (2007), p. 5340-5350. -
További szerzők:De Milito, Angelo Eidsmo, Liv Atlas, Ann Federici, Cristina Matarrese, Paola Logozzi, Mariantonia Mackall, Crystal L. Fais, Stefano Chiodi, Francesca Rajnavölgyi Éva (1950-) (immunológus) Réthi Bence (1973-) (biológus, immunológus) Vivar, Nancy Fry, Terry J.
Internet cím:elektronikus változat
elektronikus változat
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3.

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
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4.

001-es BibID:BIBFORM057877
Első szerző:Gogolák Péter (biológus, immunológus)
Cím:Targeting dendritic cells for priming cellular immune responses / Péter Gogolák, Bence Réthi, György Hajas, Éva Rajnavölgyi
Dátum:2003
ISSN:0952-3499
Megjegyzések:The cardinal role of dendritic cells (DC) in priming adaptive immunity and in orchestrating immune responses against all classes of pathogens and also against tumors is well established. Their unique potential both to maintain self-tolerance and to initiate protective immune responses against foreign and/or dangerous structures is based on the functional diversity and flexibility of these cells. Tissue DC lining antigenic portals such as mucosal surfaces and the skin are specialized to take up a wide array of compounds including proteins, lipids, carbohydrates, glycoproteins, glycolipids and oligonucleotides, particles carrying such structures and apoptotic or necrotic cells. This process is facilitated by specialized receptors with high endocytic capacity, which provides potential targets for delivering designed molecules. The best route for targeting B- and/or T cell epitopes, however, is still the subject of intense investigation. Immature DC, which reside in various tissues, can be activated by pathogens, stress and inflammation or modified metabolic products, which induce mobilization of cells to draining lymph nodes where they act as highly potent professional antigen presenting cells. This is brought about by the ability to present their accumulated intracellular content for both CD4+ helper (Th) and CD8+ cytotoxic/cytolytic T lymphocytes (Tc/CTL). Engulfed proteins are processed intracellularly and their peptide fragments are transported to the cell surface in the context of major histocompatibility complex encoded class I and II molecules for presentation to Th cells and CTLs, respectively. The T cell priming capacity of DC, however, depends not only on antigen presentation but also on other features of DC. Human monocyte-derived DC provide an excellent tool to study the internalizing, antigen-presenting and T cell-activating functions of DC at their immature and activated differentiation states. These biological activities of DC, however, are highly dependent on their migratory potential from the peripheral non-lymphoid tissues to the lymph nodes, on the expression of adhesion molecules, which support the interaction of DC with T lymphocytes, and the cytokines secreted by DC, which polarize immune responses to Th1-mediated cellular or Th2-mediated antibody responses. These results altogether demonstrate that monocyte-derived DC are useful candidates for in vitro or in vivo targeting of antigens to induce efficient adaptive immune responses against pathogens and also against tumors.
Tárgyszavak:Természettudományok Biológiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal of Molecular Recognition. - 16 : 5 (2003), p. 299-317. -
További szerzők:Réthi Bence (1973-) (biológus, immunológus) Hajas György (1970-) (biológus) Rajnavölgyi Éva (1950-) (immunológus)
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5.

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
DOI
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6.

001-es BibID:BIBFORM004837
Első szerző:Hajas György (biológus)
Cím:New phenotypic, functional and electrophysiological characteristics of KG-1 cells / György Hajas, Emese Zsiros, Tünde László, Péter Hajdú, Sándor Somodi, Bence Réthi, Péter Gogolák, Katalin Ludányi, György Panyi, Éva Rajnavölgyi
Dátum:2004
Megjegyzések:Myeloid dendritic cells (DC) are representatives of a rare and phenotypically diverse population of professional antigen presenting cells possessing high functional heterogeneity and flexibility. Here we studied the phenotypic, functional and electrophysiological characteristics of KG-1 cells, an erythroleukemia model cell line, which shares morphological and physiological similarities with immature and mature myeloid DC. We compared the expression of internalizing receptors and other cell surface molecules, antigen uptake and migration of unstimulated and activated KG-1 cells with the characteristics of immature and mature DC. Unstimulated KG-1 cells were less potent in capturing extracellular materials than immature DC. In contrast to monocyte-derived DC KG-1 cells stimulated by PMA and ionomycin ceased to migrate along the MIP-3beta chemokine gradient despite their high expression of CCR7 chemokine receptor and MDR, a transporter implicated in DC migration. Moreover, we determined the ion channel repertoire of KG-1 cells before and after treatment with PMA and ionomycin by using the patch-clamp technique. We found that both unstimulated and activated KG-1 cells expressed time- and voltage-independent, ChTx sensitive intracellular Ca(2+)-gated potassium conductance suggesting the presence of K(Ca) channels in their membranes. Based on our results we propose that KG-1 cells resemble myeloid DC but also possess unique phenotypic, functional and electrophysiological characteristics.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
analogs and derivatives
Animals
Calcium
Cell Line
Cell Movement
Cells
Dendritic Cells
Dextrans
Fluorescein
Fluorescein-5-isothiocyanate
Humans
Hungary
immunology
Ionomycin
Isoquinolines
Leukemia,Erythroblastic,Acute
metabolism
Patch-Clamp Techniques
physiology
Potassium
Research
Support
Tumor Cells,Cultured
Megjelenés:Immunology Letters. - 92 : 1-2 (2004), p. 97-106. -
További szerzők:Zsíros Emese (1980-) (orvos) László Tünde Hajdu Péter (1975-) (biofizikus) Somodi Sándor (1977-) (belgyógyász) Réthi Bence (1973-) (biológus, immunológus) Gogolák Péter (1968-) (biológus, immunológus) Ludányi Katalin (1975-) (immunológus) Panyi György (1966-) (biofizikus) Rajnavölgyi Éva (1950-) (immunológus)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
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7.

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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8.

001-es BibID:BIBFORM049591
Első szerző:Nasi, Aikaterini
Cím:Dendritic cell reprogramming by endogenously produced lactic acid / Aikaterini Nasi, Tünde Fekete, Akilan Krishnamurthy, Stuart Snowden, Eva Rajnavölgyi, Anca I. Catrina, Craig E. Wheelock, Nancy Vivar, Bence Rethi
Dátum:2013
ISSN:0022-1767 1550-6606
Megjegyzések:The demand for controlling T cell responses via dendritic cell (DC) vaccines initiated a quest for reliable and feasible DC modulatory strategies that would facilitate cytotoxicity against tumors or tolerance in autoimmunity. We studied endogenous mechanisms in developing monocyte-derived DCs (MoDCs) that can induce inflammatory or suppressor programs during differentiation, and we identified a powerful autocrine pathway that, in a cell concentration-dependent manner, strongly interferes with inflammatory DC differentiation. MoDCs developing at low cell culture density have superior ability to produce inflammatory cytokines, to induce Th1 polarization, and to migrate toward the lymphoid tissue chemokine CCL19. On the contrary, MoDCs originated from dense cultures produce IL-10 but no inflammatory cytokines upon activation. DCs from high-density cultures maintained more differentiation plasticity and can develop to osteoclasts. The cell concentration-dependent pathway was independent of peroxisome proliferator-activated receptor gamma (PPAR gamma), a known endogenous regulator of MoDC differentiation. Instead, it acted through lactic acid, which accumulated in dense cultures and induced an early and long-lasting reprogramming of MoDC differentiation. Our results suggest that the lactic acid-mediated inhibitory pathway could be efficiently manipulated in developing MoDCs to influence the immunogenicity of DC vaccines.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
myeloid suppressor-cells
par-gamma
cancer-immunotherapy
differentitation
activation
expression
environment
metabolism
carcinoma
migration
Doktori iskola
Megjelenés:Journal of Immunology. - 191 : 6 (2013), p. 3090-3099. -
További szerzők:Fekete Tünde (1984-) (immunológus, molekuláris biológus, mikrobiológus) Krishnamurthy, Akilan Snowden, Stuart Rajnavölgyi Éva (1950-) (immunológus) Catrina, Anca I. Wheelock, Craig E. Vivar, Nancy Réthi Bence (1973-) (biológus, immunológus)
Pályázati támogatás:TÁMOP-4.2.2/B-10/1-2010-0024
TÁMOP
Molekuláris Sejt- és Immunbiológiai Doktori Iskola
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9.

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
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10.

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
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11.

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
Borító:

12.

001-es BibID:BIBFORM086897
Első szerző:Réthi Bence (biológus, immunológus)
Cím:CD150 (SLAM) modulates TLR and CD40 pathways in monocyte-derived dendritic cells / Réthi Bence, Gogolák Péter, Rajnavölgyi Éva, Terhorst C., Lányi Árpád
Dátum:2005
ISSN:1521-6616
Tárgyszavak:Orvostudományok Klinikai orvostudományok idézhető absztrakt
folyóiratcikk
Megjelenés:Clinical Immunology. - 115 : Suppl1 (2005), p. S26-S26. -
További szerzők:Gogolák Péter (1968-) (biológus, immunológus) Rajnavölgyi Éva (1950-) (immunológus) Terhorst, Cox Lányi Árpád (1962-) (biológus, immunológus)
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DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:
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