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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:BIBFORM068268
035-os BibID:(cikkazonosító)427 (WoS)000399425000003 (Scopus)85018375753
Első szerző:Bene Krisztián (Biológus)
Cím:Gut Microbiota Species Can Provoke both Inflammatory and Tolerogenic Immune Responses in Human Dendritic Cells Mediated by Retinoic Acid Receptor Alpha Ligation / Krisztian Bene, Zsofia Varga, Viktor O. Petrov, Nadiya Boyko, Eva Rajnavolgyi
Dátum:2017
Megjegyzések:Dendritic cells are considered as the main coordinators of both mucosal and systemic immune responses, thus playing a determining role in shaping the outcome of effector cell responses. However, it is still uncovered how primary human monocyte-derived DC (moDC) populations drive the polarization of helper T (Th) cells in the presence of commensal bacteria harboring unique immunomodulatory properties. Furthermore,the individual members of the gut microbiota have the potential to modulate the outcomeof immune responses and shape the immunogenicity of differentiating moDCsvia the activation of retinoic acid receptor alpha (RAR?). Here, we report that moDCs are able to mediate robust Th1 and Th17 responses upon stimulation by Escherichiacoli Schaedler or Morganella morganii, while the probiotic Bacillus subtilis strain limits this effect. Moreover, physiological concentrations of all-trans retinoic acid (ATRA) are able to re-program the differentiation of moDCs resulting in altered gene expression profiles of the master transcription factors RAR? and interferon regulatory factor 4, andconcomitantly regulate the cell surface expression levels of CD1 proteins and also the mucosa-associated CD103 integrin to different directions. It was also demonstrated that the ATRA-conditioned moDCs exhibited enhanced pro-inflammatory cytokine secretion while reduced their co-stimulatory and antigen-presenting capacity thus reducing Th1 and presenting undetectable Th17 type responses against the tested microbiota strains.Importantly, these regulatory circuits could be prevented by the selective inhibition of RAR? functionality. These results altogether demonstrate that selected commensal bacterialstrains are able to drive strong effector immune responses by moDCs, while in the presence of ATRA, they support the development of both tolerogenic and inflammatory moDC in a RAR?-dependent manner.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
immunológia
mikrobiológia
dendritikus sejt
mikrobióta
A-vitamin
retinsav
T sejt
Megjelenés:Frontiers in Immunology. - 8 : 427 (2017), p. 1-17. -
További szerzők:Varga Zsófia (1992-) (molekuláris biológus) Petrov, Viktor O. Boyko, Nadiya V. Rajnavölgyi Éva (1950-) (immunológus)
Pályázati támogatás:TAMOP 4.2.4.A/2-11-1- 2012-0001
TÁMOP
TAMOP 4.2.2.A-11/1/KONV-2012-0023
TÁMOP
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3.

001-es BibID:BIBFORM065600
Első szerző:Buzás Edit
Cím:Differential Recognition of Altered Peptide Ligands Distinguishes Two Functionally Discordant (Arthritogenic and Nonarthritogenic) Autoreactive T Cell Hybridoma Clones / Edit I. Buzás, Anita Hanyecz, Yanal Murad, Ferenc Hudecz, Eva Rajnavölgyi, Katalin Mikecz, Tibor T. Glant
Dátum:2003
ISSN:0022-1767 1550-6606
Megjegyzések:Intravenous injection of a cartilage proteoglycan (aggrecan)-specific Th1 hybridoma clone 5/4E8 induced joint lesions similar to those seen in either primary or adoptively transferred arthritis in BALB/c mice. A sister clone, TA20, recognizing the same peptide epitope of human aggrecan and using the same Vbeta4 and Valpha1 segments, failed to induce joint inflammation. This study examines the fine epitope specificities of these two clones. Both 5/4E8 and TA20 hybridomas were generated using T cells from the same arthritic animal that has been immunized with human aggrecan, and both clones recognized peptides containing a consensus GRVRVNSAY sequence. However, flanking regions outside this nonapeptide sequence region had differential impact on peptide recognition by the two clones. Similarly, when single amino acid substitutions were introduced to the consensus sequence, significant differences were detected in the epitope recognition patterns of the T cell hybridomas. The 5/4E8 hybridoma showed greater flexibility in recognition, including a higher responsiveness to the corresponding self (mouse) aggrecan peptide, and produced more inflammatory cytokines (IFN-gamma and TNF-alpha), whereas hybridoma TA20 produced IL-5 in response to either human or mouse self peptide stimulation. These results demonstrate that, within the pool of immunodominant (foreign) peptide-activated lymphocytes, marked individual differences of degeneracy exist in T cell recognition, with possible implications to autopathogenic T cell functions
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal Of Immunology. - 171 : 6 (2003), p. 3025-3033. -
További szerzők:Hanyecz Anita Murad, Yanal M. Hudecz Ferenc Rajnavölgyi Éva (1950-) (immunológus) Mikecz Katalin Glant Tibor T.
Pályázati támogatás:AR40310/AR/NIAMS NIH HHS/United States
Egyéb
AR45652/AR/NIAMS NIH HHS/United States
Egyéb
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4.

001-es BibID:BIBFORM055872
Első szerző:Csillag Anikó (immunológus, biológus, angol-magyar szakfordító)
Cím:Pollen-induced oxidative stress activates dendritic cells / Csillag Anikó, Boldogh István, Pázmándi Kitti, Magyarics Zoltán, Rajnavölgyi Éva, Bácsi Attila
Dátum:2009
Tárgyszavak:Természettudományok Biológiai tudományok idézhető absztrakt
Megjelenés:Journal of Allergy and Clinical Immunology. - 123 (2009), p. S140. -
További szerzők:Boldogh István Pázmándi Kitti Linda (1984-) (molekuláris biológus, immunológus) Magyarics Zoltán (1982-) (immunológus) Rajnavölgyi Éva (1950-) (immunológus) Bácsi Attila (1967-) (immunológus)
Borító:

5.

001-es BibID:BIBFORM014049
Első szerző:Csillag Anikó (immunológus, biológus, angol-magyar szakfordító)
Cím:Pollen-Induced Oxidative Stress Influences Both Innate and Adaptive Immune Responses via Altering Dendritic Cell Functions / Csillag, A., Boldogh, I., Pazmandi, K., Magyarics, Z., Gogolak, P., Sur, S., Rajnavolgyi, E., Bacsi, A.
Dátum:2010
ISSN:0022-1767
Megjegyzések:It has been demonstrated that pollen grains contain NAD(P)H oxidases that induce oxidative stress in the airways, and this oxidative insult is critical for the development of allergic inflammation in sensitized mice. On the basis of this observation, we have examined whether pollen grain exposure triggers oxidative stress in dendritic cells (DCs), altering their functions. To test this hypothesis, human monocyte-derived DCs were treated with ragweed pollen grains. Our findings show that exposure to pollen grains induces an increase in the intracellular levels of reactive oxygen species in DCs. Our data also indicate that besides the NAD(P)H oxidases, other component(s) of pollen grains contributes to this phenomenon. Elevated levels of intracellular reactive oxygen species triggered the production of IL-8 as well as proinflammatory cytokines, such as TNF-alpha and IL-6. Treatment with pollen grains initiated the maturation of DCs, strongly upregulated the membrane expression of CD80, CD86, CD83, and HLA-DR, and caused only a slight increase in the expression of CD40. The pollen-treated DCs induced the development of naive T lymphocytes toward effector T cells with a mixed profile of cytokine production. Antioxidant inhibited both the phenotypic and functional changes of DCs, underlining the importance of oxidative stress in these processes. Collectively, these data show that pollen exposure-induced oxidative stress may contribute to local innate immunity and participate in the initiation of adaptive immune responses to pollen Ags.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Allergic Airway Inflammation
Exhaust Particle Chemicals
Tight Junctions
NADPH Oxidase
T-Cells
Maturation
Phytoprostanes
Proteins
Extracts
Gamma
Megjelenés:Journal of Immunology. - 184 : 5 (2010), p. 2377-2385. -
További szerzők:Boldogh István Pázmándi Kitti Linda (1984-) (molekuláris biológus, immunológus) Magyarics Zoltán (1982-) (immunológus) Gogolák Péter (1968-) (biológus, immunológus) Sur, Sanjiv Rajnavölgyi Éva (1950-) (immunológus) Bácsi Attila (1967-) (immunológus)
Pályázati támogatás:NK 72937
OTKA
GVOP-3.1.1.-2004-05-0393/3.0
Egyéb
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6.

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
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7.

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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8.

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
Borító:

9.

001-es BibID:BIBFORM057826
Első szerző:Fodor Mariann (szemész)
Cím:Effects of awakening and the use of topical dexamethasone and levofloxacin on the cytokine levels in tears following corneal transplantation / Mariann Fodor, Goran Petrovski, Dorottya Pásztor, Péter Gogolák, Éva Rajnavölgyi, András Berta
Dátum:2014
ISSN:2314-8861 2314-7156
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
tears
Megjelenés:Journal of Immunology Research. - 2014 (2014), p. 1-8. -
További szerzők:Petrovski, Goran (1975-) (orvos) Pásztor Dorottya (1989-) (szemész) Gogolák Péter (1968-) (biológus, immunológus) Rajnavölgyi Éva (1950-) (immunológus) Berta András (1955-) (szemész, gyermekszemész)
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10.

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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11.

001-es BibID:BIBFORM072879
Első szerző:Hancz Dóra
Cím:Flagellin increases death receptor-mediated cell death in a RIP1-dependent manner / Hancz Dora, Szabo Aniko, Molnar Tamás, Varga Zsofia, Hancz Aniko, Gregus Andrea, Hueber Anne-Odile, Rajnavolgyi Eva, Koncz Gabor
Dátum:2018
ISSN:0165-2478
Megjegyzések:Efficient adjuvants have the potential to trigger both innate and adaptive immune responses simultaneously. Flagellin is a unique pathogen-derived protein, which is recognized by pattern recognition receptors (PRRs) as well as by B-cell and T cell receptors thus providing an important link between innate and adaptive immunity. The aforementioned properties define flagellin as an optimal adjuvant. The induction of immunogenic cell death could be an additional expectation for adjuvants in the context of cancer immunotherapy due to their ability to activate dendritic cells (DC) to present tumor antigens through the engulfment of dying cells. The immunostimulatory potential of flagellin in the course of DC and lymphocyte activation is well documented, however the exact mechanism is not fully explored. Based on this limitation we sought to investigate the potential modulatory effects of flagellin on various cell death processes knowing that it plays detrimental roles in regulating the final outcome of various types of immune responses. Here we provide evidence that the pre-treatment of Jurkat T-cells with recombinant flagellin is able to increase the degree of cell death provoked by FasL or TNF-?, and concomitantly increases the cytotoxic potential of phytohemagglutinin activated T-lymphocytes in a TLR5 dependent way. In contrast to these flagellin-mediated effects on the death receptor-induced signaling events, the mitochondrial apoptotic pathway remained unaffected. Furthermore, the cell culture supernatant of wild type Salmonella enteritidis bacteria, but not their flagellin deficient variant, was able to enhance the Fas-induced cell death process. To define the molecular mechanisms of flagellin-mediated elevated levels of cell death we were able to detect the upregulation of RIP1-dependent signaling events. These findings demonstrate that the cooperative actions of pattern recognition and different death receptors are able to initiate the cell death process with the mobilization of RIP-dependent cell death modalities. This finding highlights the capability of flagellin to act as a potential adjuvant which is relevant for tumor immunotherapy.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Adjuvant
Apoptosis
Necroptosis
PAMP
T cell
TLR
Megjelenés:Immunology Letters. - 193 (2018), p. 42-50. -
További szerzők:Szabó Anikó Molnár Tamás (1989-) (molekuláris biológus) Varga Zsófia (1992-) (molekuláris biológus) Hancz Anikó Gregus Andrea (1980-) (biológus) Hueber, Anne-Odile Rajnavölgyi Éva (1950-) (immunológus) Koncz Gábor (1970-) (biológus, immunológus)
Pályázati támogatás:OTKA-114423
OTKA
GINOP-2.3.2-15-2016-00050
GINOP
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12.

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
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