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1.

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
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2.

001-es BibID:BIBFORM094223
Első szerző:Molnár Tamás (molekuláris biológus)
Cím:Caspase-9 acts as a regulator of necroptotic cell death / Molnár Tamás, Pallagi Petra, Tél Bálint, Király Róbert, Csoma Eszter, Jenei Viktória, Varga Zsófia, Gogolák Péter, Odile Hueber Anne, Máté Zoltán, Erdélyi Ferenc, Szabó Gábor, Pettkó-Szandtner Aladár, Bácsi Attila, Virág László, Maléth József, Koncz Gábor
Dátum:2021
ISSN:1742-464X
Megjegyzések:Necroptosis is a regulated necrotic-like cell death modality which has come into the focus of attention since it is known to contribute to the pathogenesis of many inflammatory and degenerative diseases as well as to tumor regulation. Based on current data, necroptosis serves as a backup mechanism when death receptor-induced apoptosis is inhibited or absent. However, the necroptotic role of the proteins involved in mitochondrial apoptosis has not been investigated. Here, we demonstrated that the stimulation of several death and pattern recognition receptors induced necroptosis under caspase-compromised conditions in wild-type, but not in caspase- 9-negative human Jurkat and murine MEF cells. Cerulein-induced pancreatitis was significantly reduced in mice with acinar cell-restricted caspase-9 gene knockout. The absence of caspase-9 led to impaired association of receptor-interacting serine/threonine-protein kinase 1 (RIPK1) and RIPK3 and resulted in decreased phosphorylation of RIP kinases, but the overexpression of RIPK1 or RIPK3 rescued the effect of caspase-9 deficiency. Inhibition of either Aurora kinase A (AURKA) or its known substrate, glycogen synthase kinase 3b (GSK3?) restored necroptosis sensitivity of caspase-9-deficient cells, indicating an interplay between caspase-9 and AURKA-mediated pathways to regulate necroptosis. Our findings suggest that caspase-9 acts as a newly identified regulator of necroptosis, and thus, caspase-9 provides a promising therapeutic target to manipulate the immunological outcome of cell death.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Caspase-9
cell death
inflammation
necroptosis
pancreatitis
Megjelenés:Febs Journal. - 288 : 22 (2021), p. 6476-6491. -
További szerzők:Pallagi Petra Tél Bálint Király Róbert (1975-) (biológus) Csoma Eszter (1978-) (molekuláris biológus, mikrobiológus) Jenei Viktória (1997-) (biológus) Varga Zsófia (1992-) (molekuláris biológus) Gogolák Péter (1968-) (biológus, immunológus) Odile Hueber, Anne Máté Zoltán Erdélyi Ferenc Szabó Gábor (budapesti orvos) Pettkó-Szandtner Aladár Bácsi Attila (1967-) (immunológus) Virág László (1965-) (biokémikus, sejtbiológus, farmakológus) Maléth József Koncz Gábor (1970-) (biológus, immunológus)
Pályázati támogatás:GINOP-2.3.2-15-2016-00050
GINOP
NKFIH 125224
Egyéb
UNKP- 20-4
Egyéb
EFOP-3.6.3-VEKOP-16-2017-00009
EFOP
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3.

001-es BibID:BIBFORM072832
035-os BibID:(Cikkazonosító)1765 (WOS)000423430000013 (Scopus)85041329100
Első szerző:Szabó Attila (molekuláris biológus, immunológus, filozófus)
Cím:Immunomodulatory capacity of the serotonin receptor 5-HT2B in a subset of human dendritic cells / Szabo Attila, Gogolak Peter, Koncz Gabor, Foldvari Zsofia, Pazmandi Kitti, Miltner Noemi, Poliska Szilard, Bacsi Attila, Djurovic Srdjan, Rajnavolgyi Eva
Dátum:2018
ISSN:2045-2322
Megjegyzések:Serotonin is a monoamine neurotransmitter that signals through a wide array of receptors (5-HT1-7) many of which are also involved in immune processes. Dendritic cells (DCs) are crucial players in immune defense by bridging innate and adaptive immune responses via their vast repertoire of pattern recognition receptors and antigen-presenting capability. Although serotonin is known to influence immunity at many levels, cell type-specific expression and function of its receptors remains poorly understood. Here we aimed to study 5-HT1-7 expression and function in CD1a- and CD1a+ human monocyte-derived DCs (moDCs). We found that the 5-HT2B receptor-subtype is solely expressed by the inflammatory CD1a+ moDC subset. Specific 5-HT2B activation potently inhibited TLR2, TLR3, and TLR7/8-induced proinflammatory cytokine and chemokine (TNF-?, IL-6, IL-8, IP-10, IL-12) but not type I interferon-? responses. 5-HT2B agonism also interfered with the polarization of CD1a+ moDC-primed CD4+ T cells towards inflammatory Th1 and Th17 effector lymphocytes. Here we report the subset-specific expression and immunomodulatory function of 5-HT2B in human moDCs. Our results expand the biological role of 5-HT2B which may act not only as a neurotransmitter receptor, but also as an important modulator of both innate and adaptive immune responses.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Scientific Reports. - 8 (2018), p. 1-12. -
További szerzők:Gogolák Péter (1968-) (biológus, immunológus) Koncz Gábor (1970-) (biológus, immunológus) Földvári Zsófia Pázmándi Kitti Linda (1984-) (molekuláris biológus, immunológus) Miltner Noémi (1990-) (molekuláris biológus) Póliska Szilárd (1978-) (biológus) Bácsi Attila (1967-) (immunológus) Djurovic, Srdjan Rajnavölgyi Éva (1950-) (immunológus)
Pályázati támogatás:GINOP-2.3.2-15-2016-00050
GINOP
PEOPLE-2013-COFUND
FP7
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DOI
Intézményi repozitóriumban (DEA) tárolt változat
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