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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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001-es BibID:	BIBFORM076291
035-os BibID:	(cikkazonosító)3070 (WoS)000454093300001 (Scopus)85059796010
Első szerző:	Fekete Tünde (immunológus, molekuláris biológus, mikrobiológus)
Cím:	Human Plasmacytoid and Monocyte-Derived Dendritic Cells Display Distinct Metabolic Profile Upon RIG-I Activation / Tünde Fekete, Máté I. Sütő, Dóra Bencze, Anett Mázló, Attila Szabo, Tamas Biro, Attila Bacsi, Kitti Pázmándi
Dátum:	2018
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk
Megjelenés:	Frontiers in Immunology. - 9 (2018), p. 1-32. -
További szerzők:	Sütő Máté István (1991-) (molekuláris biológus) Bencze Dóra (1992-) Türk-Mázló Anett (1989-) (molekuláris biológus) Szabó Attila (1981-) (molekuláris biológus, immunológus, filozófus) Bíró Tamás (1968-) (élettanász) Bácsi Attila (1967-) (immunológus) Pázmándi Kitti Linda (1984-) (molekuláris biológus, immunológus)
Pályázati támogatás:	NKFIH PD 115776 NKFIH NKFIH PD 16 120887 NKFIH GINOP-2.3.2-15-2016-00050 GINOP EFOP-3.6.3-VEKOP-16-2017-00009 EFOP
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001-es BibID:	BIBFORM075433
035-os BibID:	(cikkazonosító)2314 (WoS)000446446200002 (Scopus)85055075977
Első szerző:	Fekete Tünde (immunológus, molekuláris biológus, mikrobiológus)
Cím:	Regulatory NLRs Control the RLR-Mediated Type I Interferon and Inflammatory Responses in Human Dendritic Cells / Tünde Fekete, Dora Bencze, Attila Szabo, Eszter Csoma, Tamas Biro, Attila Bacsi, Kitti Pazmandi
Dátum:	2018
ISSN:	1664-3224
Megjegyzések:	Unique members of the nucleotide-binding domain leucine-rich repeat (NLR) family have been found to regulate intracellular signaling pathways initiated by other families of pattern recognition receptors (PRR) such as Toll-like receptors (TLRs) and retinoic-acid inducible gene I (RIG-I)-like receptors (RLRs). Plasmacytoid dendritic cells (pDCs), the most powerful type I interferon (IFN) producing cells, preferentially employ endosomal TLRs to elicit antiviral IFN responses. By contrast, conventional DCs (cDCs) predominantly use cytosolic RLRs, which are constitutively expressed in them, to sense foreign nucleic acids. Previously we have reported that, though RIG-I is absent from resting pDCs, it is inducible upon TLR stimulation. In the recent study we investigated the regulatory ability of NLRs, namely NLRC5 and NLRX1 directly associated with the RLR-mediated signaling pathway in DC subtypes showing different RLR expression, particularly in pDCs, and monocyte-derived DCs (moDCs). Here we demonstrate that similarly to RLRs, NLRC5 is also inducible upon TLR9 stimulation, whereas NLRX1 is constitutively expressed in pDCs. Inhibition of NLRC5 and NLRX1 expression in pDCs augmented the RLR-stimulated expression of type I IFNs but did not affect the production of the pro-inflammatory cytokines TNF, IL-6, and the chemokine IL-8. Further we show that immature moDCs constantly express RLRs, NLRX1 and NLRC5 that are gradually upregulated during their differentiation. Similarly to pDCs, NLRX1 suppression increased the RLR-induced production of type I IFNs in moDCs. Interestingly, RLR stimulation of NLRX1-silenced moDCs leads to a significant increase in pro-inflammatory cytokine production and I?Bα degradation, suggesting increased NF-?B activity. On the contrary, NLRC5 does not seem to have any effect on the RLR-mediated cytokine responses in moDCs. In summary, our results indicate that NLRX1 negatively regulates the RLR-mediated type I IFN production both in pDCs and moDCs. Further we show that NLRX1 inhibits pro-inflammatory cytokine secretion in moDCs but not in pDCs following RLR stimulation. Interestingly, NLRC5 suppresses the RLR-induced type I IFN secretion in pDCs but does not appear to have any regulatory function on the RLR pathway in moDCs. Collectively, our work demonstrates that RLR-mediated innate immune responses are primarily regulated by NLRX1 and partly controlled by NLRC5 in human DCs.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk
Megjelenés:	Frontiers in Immunology. - 9 (2018), p. 1-19. -
További szerzők:	Bencze Dóra (1992-) Szabó Attila (1981-) (molekuláris biológus, immunológus, filozófus) Csoma Eszter (1978-) (molekuláris biológus, mikrobiológus) Bíró Tamás (1968-) (élettanász) Bácsi Attila (1967-) (immunológus) Pázmándi Kitti Linda (1984-) (molekuláris biológus, immunológus)
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM059517
035-os BibID:	(cikkazonosító)358 (WOS)000358953500001 (Scopus)84936867063
Első szerző:	Szabó Attila (molekuláris biológus, immunológus, filozófus)
Cím:	Psychedelics and Immunomodulation : novel Approaches and Therapeutic Opportunities / Attila Szabo
Dátum:	2015
ISSN:	1664-3224
Megjegyzések:	Classical psychedelics are psychoactive substances, which, besides their psychopharmacological activity, have also been shown to exert significant modulatory effects on immune responses by altering signaling pathways involved in inflammation, cellularproliferation, and cell survival via activating NF-?B and mitogen-activated protein kinases. Recently, several neurotransmitter receptors involved in the pharmacology ofpsychedelics, such as serotonin and sigma-1 receptors, have also been shown to play crucial roles in numerous immunological processes. This emerging field also offers promising treatment modalities in the therapy of various diseases including autoimmune and chronic inflammatory conditions, infections, and cancer. However, the scarcity of available review literature renders the topic unclear and obscure, mostly posingpsychedelics as illicit drugs of abuse and not as physiologically relevant molecules or as possible agents of future pharmacotherapies. In this paper, the immunomodulatorypotential of classical serotonergic psychedelics, including N,N-dimethyltryptamine (DMT), 5-methoxy-N,N-dimethyltryptamine (5-MeO-DMT), lysergic acid diethylamide (LSD), 2,5-dimethoxy-4-iodoamphetamine (DOI), and 3,4-methylenedioxy-methamphetamine (MDMA) will be discussed from a perspective of molecular immunology and pharmacology. Special attention will be given to the functional interaction of serotonin and sigma-1 receptors and their cross-talk with toll-like and RIG-I-like pattern-recognition receptor-mediated signaling. Furthermore, novel approaches will be suggested feasible for the treatment of diseases with chronic inflammatory etiology and pathology, such as atherosclerosis, rheumatoid arthritis, multiple sclerosis, schizophrenia, depression, and Alzheimer's disease.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk psychedelics innate immunity inflammation autoimmunity serotonin receptors sigma-1 receptor pattern-recognition receptors psychopharmacology
Megjelenés:	Frontiers in Immunology. - 6 (2015), p. 1-11. -
Pályázati támogatás:	TÁMOP-4.2.4.A/2-11-1-2012-0001 TÁMOP
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