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001-es BibID:	BIBFORM054305
035-os BibID:	PMID: 18243342
Első szerző:	Hancz Anikó
Cím:	Integration of signals mediated by B-cell receptor, B-cell activating factor of the tumor necrosis factor family (BAFF) and Fas (CD95) / Anikó Hancz, Zoltán Hérincs, Zsuzsa Neer, Gabriella Sármay, Gábor Koncz
Dátum:	2008
ISSN:	0165-2478
Megjegyzések:	The survival of the mature resting B cells depends on signaling from B cell receptor (BCR), and a plethora of positive and negative regulators, that maintain cellular homeostasis and ultimately determine cell's fate, i.e., survival or programmed death (apoptosis). Among these regulators we have investigated the B cell activating factor belonging to tumor necrosis factor family (BAFF) and the prototypic death receptor Fas/CD95 mediated signals. We have shown that BAFF inhibits Fas-mediated cell death, however, the BCR-driven survival signals were not strengthened by BAFF. Therefore, we propose that BAFF may function independently of the antigen specificity of BCR, thus may enhance the risk of autoimmune diseases by promoting the survival of bystander B cells in the germinal center.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban B-cell BAFF Fas apoptosis selection signaling
Megjelenés:	Immunology Letters. - 116 : 2 (2008), p. 211-217. -
További szerzők:	Hérincs Zoltán Neer Zsuzsa Sármay Gabriella Koncz Gábor (1970-) (biológus, immunológus)
Pályázati támogatás:	D48469 OTKA
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM041843
Első szerző:	Hancz Anikó
Cím:	TLR9-mediated signals rescue B-cells from Fas-induced apoptosis via inactivation of caspases / Anikó Hancz, Gábor Koncz, Dániel Szili, Gabriella Sármay
Dátum:	2012
ISSN:	0165-2478
Megjegyzések:	The death receptor, CD95/Fas, serves to eliminate potentially dangerous, self-reactive B cells. Engagement of B-cell receptors (BCR) on mature B-cells mediates the escape from cell death resulting in the activation and expansion of antigen specific clones. In addition to the antigen receptors, the receptors of B-cell activating factor belong to the tumor necrosis factor (TNF) family (BAFFR); moreover, the pattern recognition receptor, TLR9 may also deliver survival signals inhibiting Fas-mediated death of B-cells. Our aim was to compare the mechanism of BCR-induced and the BAFFR- or TLR9-stimulated rescue of B-cells from CD95/Fas-mediated apoptosis. We have found that BAFFR and TLR9 collaborate with BCR to protect B-cells from Fas-induced elimination and the rescue is independent of protein synthesis. The results revealed that the TLR9- and BCR-triggered rescue signals are transmitted through partially overlapping pathways; the protein kinase C (PKC) and the abl kinase induced phosphorylation may inactivate caspases in both CpG and anti-IgG stimulated cells. However, PI3-K activation is crucial upon the BCR driven anti-apoptotic effect, while p38 MAPK-mediated inactivation of caspases seems to play essential role in TLR9-mediated protection against Fas-induced programmed cell death.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Apoptosis BAFF B-cells Fas TLR9
Megjelenés:	Immunology Letters. - 143 : 1 (2012), p. 77-84. -
További szerzők:	Koncz Gábor (1970-) (biológus, immunológus) Szili Dániel Sármay Gabriella
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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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
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM039523
Első szerző:	Koncz Gábor (biológus, immunológus)
Cím:	Vesicles Released by Activated T Cells Induce Both Fas-Mediated RIP-Dependent Apoptotic and Fas-Independent Nonapoptotic Cell Deaths / Koncz, G., Hancz, A., Chakrabandhu, K., Gogolak, P., Kerekes, K., Rajnavolgyi, E., Hueber, Anne-Odile
Dátum:	2012
ISSN:	0022-1767
Megjegyzések:	Activated T cells secrete Fas ligand (FasL)-containing vesicles (secreted vesicles) that induce death of target cells. We provide evidence that secreted vesicles from culture supernatants (Csup) of various origins are able to generate both Fas-dependent apoptotic and Fas-independent, nonapoptotic cell death. In the absence of Fas, the nonapoptotic, Fas-independent pathway could still induce cell death. In contrast to RIP-independent classical Fas-induced cell death triggered by cross-linked or membrane-bound FasL, CSup-derived stimuli-induced apoptosis exhibited unique molecular and enzymatic characteristics. It could be partially inhibited by blocking cathepsin D enzyme activity and required the presence of RIP. Whereas stimulation with CSup, derived from both FasL-overexpressing Jurkat cells and PBMC, could induce cell death, the requirements for Fas-associated death domain protein and caspase-9 were different between the two systems. Our study highlights an important distinction between cell contact-mediated and secreted vesicle-generated activation-induced cell death and also demonstrates that the type of the secreted vesicles can also modify the cell death route. We propose that besides cell-to-cell interaction-mediated Fas triggering, stimuli induced by secreted vesicles can mediate important additional cell death signals regulating activation-induced cell death under physiological conditions.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Molekuláris Medicina
Megjelenés:	Journal Of Immunology. - 189 : 6 (2012), p. 2815-2823. -
További szerzők:	Hancz Anikó Chakrabandhu, Krittalak Gogolák Péter (1968-) (biológus, immunológus) Kerekes Krisztina Rajnavölgyi Éva (1950-) (immunológus) Hueber, Anne-Odile
Pályázati támogatás:	TÁMOP-4.2.1/B-09/1/KONV-2010-0007 TÁMOP Jelátviteli kapcsolatok ős- és dendritikus sejt altípusokban
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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