TY - JOUR AU - Horváth, Dorottya AU - Pénzes, Zsófia AU - Molnár, Petra AU - Rebenku, István AU - Vereb, György AU - Szántó, Magdolna AU - Muzsai, Szabolcs AU - Szegedi, Andrea AU - Dajnoki, Zsolt AU - Pázmándi, Kitti Linda AU - Fekete, Tünde AU - Bácsi, Attila AU - Szöllősi, Attila TI - Natriuretic peptides modulate monocyte-derived Langerhans cell differentiation and promote a migratory phenotype JF - FRONTIERS IN IMMUNOLOGY J2 - FRONT IMMUNOL VL - 16 PY - 2025 SP - 1 EP - 14 PG - 14 SN - 1664-3224 DO - 10.3389/fimmu.2025.1593141 UR - https://m2.mtmt.hu/api/publication/36188415 ID - 36188415 LA - English DB - MTMT ER - TY - JOUR AU - Pázmándi, Kitti Linda AU - Ágics, Beatrix AU - Szöllősi, Attila AU - Bácsi, Attila AU - Fekete, Tünde TI - Ginger-derived bioactive compounds attenuate the Toll-like receptor mediated responses of human dendritic cells JF - EUROPEAN JOURNAL OF PHARMACOLOGY J2 - EUR J PHARMACOL VL - 967 PY - 2024 SN - 0014-2999 DO - 10.1016/j.ejphar.2024.176399 UR - https://m2.mtmt.hu/api/publication/34720432 ID - 34720432 LA - English DB - MTMT ER - TY - JOUR AU - Pázmándi, Kitti Linda AU - Szöllősi, Attila AU - Fekete, Tünde TI - The “root” causes behind the anti-inflammatory actions of ginger compounds in immune cells JF - FRONTIERS IN IMMUNOLOGY J2 - FRONT IMMUNOL VL - 15 PY - 2024 PG - 17 SN - 1664-3224 DO - 10.3389/fimmu.2024.1400956 UR - https://m2.mtmt.hu/api/publication/35079207 ID - 35079207 AB - Ginger ( Zingiber officinale ) is one of the most well-known spices and medicinal plants worldwide that has been used since ancient times to treat a plethora of diseases including cold, gastrointestinal complaints, nausea, and migraine. Beyond that, a growing body of literature demonstrates that ginger exhibits anti-inflammatory, antioxidant, anti-cancer and neuroprotective actions as well. The beneficial effects of ginger can be attributed to the biologically active compounds of its rhizome such as gingerols, shogaols, zingerone and paradols. Among these compounds, gingerols are the most abundant in fresh roots, and shogaols are the major phenolic compounds of dried ginger. Over the last two decades numerous in vitro and in vivo studies demonstrated that the major ginger phenolics are able to influence the function of various immune cells including macrophages, neutrophils, dendritic cells and T cells. Although the mechanism of action of these compounds is not fully elucidated yet, some studies provide a mechanistic insight into their anti-inflammatory effects by showing that ginger constituents are able to target multiple signaling pathways. In the first part of this review, we summarized the current literature about the immunomodulatory actions of the major ginger compounds, and in the second part, we focused on the possible molecular mechanisms that may underlie their anti-inflammatory effects. LA - English DB - MTMT ER - TY - JOUR AU - Pénzes, Zsófia AU - Horváth, Dorottya AU - Molnár, Petra AU - Fekete, Tünde AU - Pázmándi, Kitti Linda AU - Bácsi, Attila AU - Szöllősi, Attila TI - Anandamide modulation of monocyte-derived Langerhans cells: implications for immune homeostasis and skin inflammation JF - FRONTIERS IN IMMUNOLOGY J2 - FRONT IMMUNOL VL - 15 PY - 2024 SP - 1 EP - 16 PG - 16 SN - 1664-3224 DO - 10.3389/fimmu.2024.1423776 UR - https://m2.mtmt.hu/api/publication/35149243 ID - 35149243 LA - English DB - MTMT ER - TY - JOUR AU - Bencze, Dóra AU - Fekete, Tünde AU - Pázmándi, Kitti Linda TI - Correlation between Type I Interferon Associated Factors and COVID-19 Severity JF - INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES J2 - INT J MOL SCI VL - 23 PY - 2022 IS - 18 SN - 1661-6596 DO - 10.3390/ijms231810968 UR - https://m2.mtmt.hu/api/publication/33104558 ID - 33104558 N1 - Funding Agency and Grant Number: National Research, Development and Innovation Office [NKFIH FK 128294, NKFIH PD 135193]; European Union; European Regional Development Fund; New National Excellence Program of the Ministry for Innovation and Technology from the source of the National Research, Development and Innovation Fund [UNKP-21-05-DE-170, UNKP-21-3-II-DE-21]; Janos Bolyai Research Scholarship from the Hungarian Academy of Sciences [bo_122_19]; [GINOP-2.3.2-15-2016-00050] Funding text: This work was supported by the National Research, Development and Innovation Office (NKFIH FK 128294 to K.P., NKFIH PD 135193 to T.F.). The work was also supported by GINOP-2.3.2-15-2016-00050 project. The project is co-financed by the European Union and the European Regional Development Fund. K.P. and D.B. were supported by UNKP-21-05-DE-170 and UNKP-21-3-II-DE-21 New National Excellence Program of the Ministry for Innovation and Technology from the source of the National Research, Development and Innovation Fund. K.P. was further supported by the Janos Bolyai Research Scholarship from the Hungarian Academy of Sciences (bo_122_19). AB - Antiviral type I interferons (IFN) produced in the early phase of viral infections effectively inhibit viral replication, prevent virus-mediated tissue damages and promote innate and adaptive immune responses that are all essential to the successful elimination of viruses. As professional type I IFN producing cells, plasmacytoid dendritic cells (pDC) have the ability to rapidly produce waste amounts of type I IFNs. Therefore, their low frequency, dysfunction or decreased capacity to produce type I IFNs might increase the risk of severe viral infections. In accordance with that, declined pDC numbers and delayed or inadequate type I IFN responses could be observed in patients with severe coronavirus disease (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), as compared to individuals with mild or no symptoms. Thus, besides chronic diseases, all those conditions, which negatively affect the antiviral IFN responses lengthen the list of risk factors for severe COVID-19. In the current review, we would like to briefly discuss the role and dysregulation of pDC/type I IFN axis in COVID-19, and introduce those type I IFN-dependent factors, which account for an increased risk of COVID-19 severity and thus are responsible for the different magnitude of individual immune responses to SARS-CoV-2. LA - English DB - MTMT ER - TY - JOUR AU - Bencze, Dóra AU - Fekete, Tünde AU - Pfliegler, Valter Péter AU - Szöőr, Árpád AU - Csoma, Eszter AU - Szántó, Antónia AU - Tarr, Tünde AU - Bácsi, Attila AU - Kemény, Lajos AU - Veréb, Zoltán AU - Pázmándi, Kitti Linda TI - Interactions between the NLRP3-Dependent IL-1β and the Type I Interferon Pathways in Human Plasmacytoid Dendritic Cells JF - INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES J2 - INT J MOL SCI VL - 23 PY - 2022 IS - 20 PG - 34 SN - 1661-6596 DO - 10.3390/ijms232012154 UR - https://m2.mtmt.hu/api/publication/33225737 ID - 33225737 N1 - Funding Agency and Grant Number: NKFIH [FK 128294, GINOP-2.3.2-15-2016-00050]; New National Excellence Program of the Ministry for Innovation and Technology [UNKP-21-05-DE-170, UNKP-21-3-II-DE-21]; Hungarian Academy of Sciences [bo_122_19] Funding text: The work was supported by NKFIH FK 128294 and GINOP-2.3.2-15-2016-00050 projects, UNKP-21-05-DE-170 and UNKP-21-3-II-DE-21 New National Excellence Program of the Ministry for Innovation and Technology managed by the National Research, Development and Innovation Office and the Janos Bolyai Research Scholarship from the Hungarian Academy of Sciences bo_122_19). AB - Generally, a reciprocal antagonistic interaction exists between the antiviral type I interferon (IFN) and the antibacterial nucleotide-binding oligomerization domain (NOD)-like receptor pyrin domain containing 3 (NLRP3)-dependent IL-1β pathways that can significantly shape immune responses. Plasmacytoid dendritic cells (pDCs), as professional type I IFN-producing cells, are the major coordinators of antiviral immunity; however, their NLRP3-dependent IL-1β secretory pathway is poorly studied. Our aim was to determine the functional activity of the IL-1β pathway and its possible interaction with the type I IFN pathway in pDCs. We found that potent nuclear factor-kappa B (NF-κB) inducers promote higher levels of pro-IL-1β during priming compared to those activation signals, which mainly trigger interferon regulatory factor (IRF)-mediated type I IFN production. The generation of cleaved IL-1β requires certain secondary signals in pDCs and IFN-α or type I IFN-inducing viruses inhibit IL-1β production of pDCs, presumably by promoting the expression of various NLRP3 pathway inhibitors. In line with that, we detected significantly lower IL-1β production in pDCs of psoriasis patients with elevated IFN-α levels. Collectively, our results show that the NLRP3-dependent IL-1β secretory pathway is inducible in pDCs; however, it may only prevail under inflammatory conditions, in which the type I IFN pathway is not dominant. LA - English DB - MTMT ER - TY - JOUR AU - Bencze, Dóra AU - Fekete, Tünde AU - Pázmándi, Kitti Linda TI - Type I Interferon Production of Plasmacytoid Dendritic Cells under Control JF - INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES J2 - INT J MOL SCI VL - 22 PY - 2021 IS - 8 SN - 1661-6596 DO - 10.3390/ijms22084190 UR - https://m2.mtmt.hu/api/publication/32008413 ID - 32008413 N1 - Funding Agency and Grant Number: National Research, Development and Innovation OfficeNational Research, Development & Innovation Office (NRDIO) - Hungary [NKFIH FK 128294, NKFIH PD 135193]; European UnionEuropean Commission; European Regional Development FundEuropean Commission; New National Excellence Program of the Ministry for Innovation and Technology from the National Research, Development and Innovation Fund [UNKP-20-05-DE-3]; Janos Bolyai Research Scholarship from the Hungarian Academy of Sciences; [GINOP2.3.2-15-2016-00050] Funding text: This work was supported by the National Research, Development and Innovation Office (NKFIH FK 128294 to K.P., NKFIH PD 135193 to T.F.). The work was also supported by GINOP2.3.2-15-2016-00050 project. The project is co-financed by the European Union and the European Regional Development Fund. K.P. was also supported by UNKP-20-05-DE-3 New National Excellence Program of the Ministry for Innovation and Technology from the source of the National Research, Development and Innovation Fund and the Janos Bolyai Research Scholarship from the Hungarian Academy of Sciences. LA - English DB - MTMT ER - TY - JOUR AU - Bencze, Dóra AU - Fekete, Tünde AU - Pázmándi, Kitti Linda TI - Az I-es típusú interferonok jelentősége COVID-19-ben JF - IMMUNOLÓGIAI SZEMLE J2 - IMMUNOLÓGIAI SZEMLE VL - 13 PY - 2021 IS - 2 SP - 26 EP - 49 PG - 24 SN - 2061-0203 UR - https://m2.mtmt.hu/api/publication/32075885 ID - 32075885 LA - Hungarian DB - MTMT ER - TY - JOUR AU - Bencze, Dóra AU - Fekete, Tünde AU - Berki-Pál, Angéla AU - Pázmándi, Kitti Linda TI - Az NLRP3 inflammaszóma aktivitásának és szabályozásának vizsgálata humán plazmacitoid dendritikus sejtekben JF - IMMUNOLÓGIAI SZEMLE J2 - IMMUNOLÓGIAI SZEMLE VL - 13 PY - 2021 IS - 3 SP - 27 SN - 2061-0203 UR - https://m2.mtmt.hu/api/publication/33104946 ID - 33104946 LA - Hungarian DB - MTMT ER - TY - JOUR AU - Fekete, Tünde AU - Bencze, Dóra AU - Bíró, Eduárd AU - Benkő, Szilvia AU - Pázmándi, Kitti Linda TI - Focusing on the Cell Type Specific Regulatory Actions of NLRX1 JF - INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES J2 - INT J MOL SCI VL - 22 PY - 2021 IS - 3 PG - 36 SN - 1661-6596 DO - 10.3390/ijms22031316 UR - https://m2.mtmt.hu/api/publication/31927666 ID - 31927666 N1 - Department of Immunology, Faculty of Medicine, University of Debrecen, 1 Egyetem Square, Debrecen, H-4032, Hungary Doctoral School of Molecular Cell and Immune Biology, University of Debrecen, 1 Egyetem Square, Debrecen, H-4032, Hungary Department of Physiology, Faculty of Medicine, University of Debrecen, 98 Nagyerdei krt., Debrecen, H-4002, Hungary Correspondence Address: Pázmándi, K.; Department of Immunology, 1 Egyetem Square, Hungary; email: pazmandikitti@yahoo.de Funding details: European Commission, EC Funding details: Magyar Tudományos Akadémia, MTA Funding details: European Regional Development Fund, FEDER Funding details: Nemzeti Kutatási Fejlesztési és Innovációs Hivatal, NKFIH, FK 128294, GINOP-2.3.2-15-2016-00050, K 131844, PD 135193 Funding details: Nemzeti Kutatási, Fejlesztési és Innovaciós Alap, NKFIA Funding details: Ministry for Innovation and Technology Funding details: National Research, Development and Innovation Office Funding text 1: This work was supported by the National Research, Development and Innovation Office (NKFIH FK 128294 to KP, NKFIH PD 135193 to TF and NKFIH K 131844 to SB). The work was also supported by GINOP-2.3.2-15-2016-00050 project. The project is co-financed by the European Union and the European Regional Development Fund. KP was also supported by ?NKP-20-05-DE-3 New National Excellence Program of the Ministry for Innovation and Technology from the source of the National Research, Development and Innovation Fund and the J?nos Bolyai Research Scholarship from the Hungarian Academy of Sciences. AB - Cells utilize a diverse repertoire of cell surface and intracellular receptors to detect exogenous or endogenous danger signals and even the changes of their microenvironment. However, some cytosolic NOD-like receptors (NLR), including NLRX1, serve more functions than just being general pattern recognition receptors. The dynamic translocation between the cytosol and the mito-chondria allows NLRX1 to interact with many molecules and thereby to control multiple cellular functions. As a regulatory NLR, NLRX1 fine-tunes inflammatory signaling cascades, regulates mi-tochondria-associated functions, and controls metabolism, autophagy and cell death. Nevertheless, literature data are inconsistent and often contradictory regarding its effects on individual cellular functions. One plausible explanation might be that the regulatory effects of NLRX1 are highly cell type specific and the features of NLRX1 mediated regulation might be determined by the unique functional activity or metabolic profile of the given cell type. Here we review the cell type specific actions of NLRX1 with a special focus on cells of the immune system. NLRX1 has already emerged as a potential therapeutic target in numerous immune-related diseases, thus we aim to highlight which regulatory properties of NLRX1 are manifested in disease-associated dominant immune cells that presumably offer promising therapeutic solutions to treat these disorders. © 2021 by the authors. Licensee MDPI, Basel, Switzerland. LA - English DB - MTMT ER -