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001-es BibID:	BIBFORM088738
035-os BibID:	(cikkazonosító)572960 (WoS)000576009300001 (Scopus)85091480359
Első szerző:	Fekete Tünde (immunológus, molekuláris biológus, mikrobiológus)
Cím:	Regulation of RLR-Mediated Antiviral Responses of Human Dendritic Cells by mTOR / Fekete Tünde, Ágics Beatrix, Bencze Dóra, Bene Krisztián, Szántó Antónia, Tarr Tünde, Veréb Zoltán, Bácsi Attila, Pázmándi Kitti
Dátum:	2020
ISSN:	1664-3224
Megjegyzések:	To detect replicating viruses, dendritic cells (DCs) utilize cytoplasmic retinoic acid inducible gene-(RIG) I-like receptors (RLRs), which play an essential role in the subsequent activation of antiviral immune responses. In this study, we aimed to explore the role of the mammalian target of rapamycin (mTOR) in the regulation of RLR-triggered effector functions of human monocyte-derived DCs (moDCs) and plasmacytoid DCs (pDCs). Our results show that RLR stimulation increased the phosphorylation of the mTOR complex (mTORC) 1 and mTORC2 downstream targets p70S6 kinase and Akt, respectively, and this process was prevented by the mTORC1 inhibitor rapamycin as well as the dual mTORC1/C2 kinase inhibitor AZD8055 in both DC subtypes. Furthermore, inhibition of mTOR in moDCs impaired the RLR stimulation-triggered glycolytic switch, which was reflected by the inhibition of lactate production and downregulation of key glycolytic genes. Blockade of mTOR diminished the ability of RLR-stimulated moDCs and pDCs to secret type I interferons (IFNs) and pro-inflammatory cytokines, while it did not affect the phenotype of DCs. We also found that mTOR blockade decreased the phosphorylation of Tank-binding kinase 1 (TBK1), which mediates RLR-driven cytokine production. In addition, rapamycin abrogated the ability of both DC subtypes to promote the proliferation and differentiation of IFN-y and Granzyme B producing CD8 + T cells. Interestingly, AZD8055 was much weaker in its ability to decrease the T cell proliferation capacity of DCs and was unable to inhibit the DC-triggered production of IFN-y and Granyzme B by CD8 + T cells. Here we demonstrated for the first time that mTOR positively regulates the RLR-mediated antiviral activity of human DCs. Further, we show that only selective inhibition of mTORC1 but not dual mTORC1/C2 blockade suppresses effectively the T cell stimulatory capacity of DCs that should be considered in the development of new generation mTOR inhibitors and in the improvement of DC-based vaccines.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk RLR signaling T cell stimulation antiviral response dendritic cell mTOR
Megjelenés:	Frontiers in Immunology. - 11 (2020), p. 1-20. -
További szerzők:	Ágics Beatrix (1995-) Bencze Dóra (1992-) Bene Krisztián (1986-) (Biológus) Szántó Antónia (1977-) (belgyógyász, allergológus és klinikai immunológus) Tarr Tünde (1976-) (belgyógyász, allergológus és klinikai immunológus) Veréb Zoltán (1980-) (immunológus, mikrobiológus, molekuláris biológus) Bácsi Attila (1967-) (immunológus) Pázmándi Kitti Linda (1984-) (molekuláris biológus, immunológus)
Pályázati támogatás:	GINOP-2.3.2-15-2016-00050 GINOP FK 128294 NKFIH UNKP 19-4 Egyéb
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001-es BibID:	BIBFORM092150
035-os BibID:	(cikkazonosító)639975 (WoS)000635978100001 (Scopus)85103554422
Első szerző:	Szabó Krisztina (Molekuláris biológus)
Cím:	The imbalance of circulating follicular T helper cell subsets in primary Sjögren's syndrome associates with serological alterations and abnormal B-cell distribution / Krisztina Szabó, Ilona Jámbor, Antónia Szántó, Ildikó Fanny Horváth, Tünde Tarr, Britt Nakken, Péter Szodoray, Gábor Papp
Dátum:	2021
ISSN:	1664-3224
Megjegyzések:	Since B-cell hyperactivity and pathologic antibody response are key features in the immunopathogenesis of primary Sjögren's syndrome (pSS), the role of follicular T helper (TFH) cells as efficient helpers in the survival and differentiation of B cells has been emerged. Our aim was to investigate whether a change in the balance of circulating (c)TFH subsets and follicular regulatory T (TFR) cells could affect the distribution of B cells in pSS. Peripheral blood of 38 pSS patients and 27 healthy controls was assessed for the frequencies of cTFH cell subsets, TFR cells and certain B cell subpopulations by multicolor flow cytometry. Serological parameters, including anti-SSA, anti-SSB autoantibodies, immunoglobulin and immune complex titers were determined as part of the routine diagnostic evaluation. Patients with pSS showed a significant increase in activated cTFH cell proportions, which was associated with serological results. Frequencies of cTFH subsets were unchanged in pSS patients compared to healthy controls. The percentages and number of cTFR cells exhibited a significant increase in autoantibody positive patients compared to patients with seronegative pSS. The proportions of transitional and naïve B cells were significantly increased, whereas subsets of memory B cells were significantly decreased and correlated with autoantibody production. Functional analysis revealed that the simultaneous blockade of cTFH and B cell interaction with anti-IL-21 and anti-CD40 antibodies decreased the production of IgM and IgG. Imbalance in TFH subsets and TFR cells indicates an ongoing over-activated humoral immune response, which contributes to the characteristic serological manifestations and the pathogenesis of pSS.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk follicular T helper cell follicular regulatory T cell Chemokine receptors B cells primary Sjögren's syndrome
Megjelenés:	Frontiers in Immunology. - 12 (2021), p. 1-13. -
További szerzők:	Jámbor Ilona (1985-) (orvosi biotechológus) Szántó Antónia (1977-) (belgyógyász, allergológus és klinikai immunológus) Horváth Ildikó Fanny (1980-) (belgyógyász, allergológus, klinikai immunológus) Tarr Tünde (1976-) (belgyógyász, allergológus és klinikai immunológus) Nakken, Britt Szodoray Péter (1973-) (belgyógyász, orvos) Papp Gábor (1984-) (belgyógyász)
Pályázati támogatás:	121327 PD_16 124177 OTKA
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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