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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
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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