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1.

001-es BibID:BIBFORM010321
Első szerző:Dammeyer, Pascal
Cím:Vaccination with beta(2)-microglobulin-deficient dendritic cells protects against growth of beta(2)-microglobulin-deficient tumours / Pascal Dammeyer, Amos R. Mwakigonja, Réthi Bence, Francesca Chiodi, Elisabeth Wolpert
Dátum:2009
ISSN:0300-9475 (Print)
Megjegyzések:Defects in cell surface expression of major histocompatibility complex class I antigen molecules are common in tumour cells. We have previously described the generation of adaptive immunity to tumour cells deficient in the transporter associated with antigen processing molecule. In this study, we demonstrate enhanced in vivo protection against growth of beta(2)-microglobulin-deficient tumour cells in syngeneic C57Bl/6 mice, following vaccination with beta(2)-microglobulin-deficient dendritic cells. In vitro analysis suggested that vaccinated mice produced CD3+ cells, which could induce apoptosis in syngeneic beta(2)-microglobulin-deficient tumour and non-malignant cells. Further investigation of target cell recognition suggested that also tumour cells lacking expression of classical major histocompatibility complex class I heavy chains and functional transporter associated with antigen processing molecules were recognized by CD3+ effector cells from vaccinated mice. Histopathological examination of organs from vaccinated mice showed no significant vaccination-induced pathology. The present findings point to a new possible strategy to counteract the growth of major histocompatibility complex class I-deficient tumour cells.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
MHC Class-I
Natural Cytotoxicity Receptors
Antigen Processing Machinery
HIV-1 Nef Protein
Melanoma Cells
NKG2D Ligands
Heavy-Chains
T-Cells
Killer Lymphocytes
Immune-Responses
Megjelenés:Scandinavian Journal of Immunology. - 70 : 1 (2009), p. 44-52. -
További szerzők:Mwakigonja, Amos R. Réthi Bence (1973-) (biológus, immunológus) Chiodi, Francesca Wolpert, Elisabeth
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2.

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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3.

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.
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4.

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)
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5.

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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6.

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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7.

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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8.

001-es BibID:BIBFORM005817
Első szerző:Titanji, Kehmia
Cím:Altered distribution of natural killer cell subsets identified by CD56, CD27 and CD70 in primary and chronic human immunodeficiency virus-1 infection / Kehmia Titanji, Stefano Sammicheli, Angelo De Milito, Paola Mantegani, Claudio Fortis, Louise Berg, Klas Karre, Giovanna Travi, Chiara Tassandin, Lucia Lopalco, Bence Rethi, Giuseppe Tambussi, Francesca Chiodi
Dátum:2008
Megjegyzések:Human natural killer (NK) (CD3(-) CD56(+)) cells can be divided into two functionally distinct subsets, CD3(-) CD56(dim) and CD3(-) CD56(bright). We analysed the distribution of NK cell subsets in primary and chronic human immunodeficiency virus-1 (HIV-1) infection, to determine if HIV infection stage may influence the subset distribution. In primary infection, contrary to chronic infection, the CD3(-) CD56(dim) subset was expanded compared to healthy controls. We also studied the effect of antiretroviral therapy administered early in infection and found that NK cell subset distribution was partially restored after 6 months of antiretroviral therapy in primary infection, but not normalized. Recently, NK cells have been divided into CD27(-) and CD27(+) subsets with different migratory and functional capacity and CD27-mediated NK cell activation has been described in mice. We therefore investigated whether CD27 and/or CD70 (CD27 ligand) expression on NK cells, and thus the distribution of these novel NK subsets, was altered in HIV-1-infected patients. We found up-regulated expression of both CD27 and CD70 on NK cells of patients, resulting in higher proportions of CD27(high) and CD70(high) NK cells, and this phenomenon was more pronounced in chronic infection. Experiments conducted in vitro suggest that the high interleukin-7 levels found during HIV-1 infection may participate in up-regulation of CD70 on NK cell subsets. Imbalance of NK cell subsets and up-regulated expression of CD27 and CD70 initiated early in HIV-1 infection may indicate NK cell activation and intrinsic defects initiated by HIV-1 to disarm the innate immune response to the virus.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
HIV-1
CD27
CD70
NK cells
immune activation
antiretroviral therapy
Megjelenés:Immunology. - 123 : 2 (2008), p. 164-170. -
További szerzők:Sammicheli, Stefano De Milito, Angelo Mantegani, Paola Fortis, Claudio Berg, Louise Karre, Klas Travi, Giovanna Tassandin, Chiara Lopalco, Lucia Réthi Bence (1973-) (biológus, immunológus) Tambussi, Giuseppe Chiodi, Francesca
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