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001-es BibID:BIBFORM132180
035-os BibID:(scopus)105013343872 (wos)001549131500001
Első szerző:Diós Ádám (molekuláris biológus)
Cím:Anifrolumab Attenuates Follicular Helper T Cell Activation in Patients with Systemic Lupus Erythematosus / Diós Ádám, Gyetvai Ágnes, Papp Gábor, Tarr Tünde
Dátum:2025
ISSN:1661-6596 1422-0067
Megjegyzések:Systemic lupus erythematosus (SLE) is a severe autoimmune disease characterized by autoantibody production and multi-organ involvement. Anifrolumab, a monoclonal antibody targeting the type I interferon (IFN) receptor, has been approved for the treatment of SLE. Our aim was to investigate the long-term effects of inhibited type I IFN signaling on circulating follicular helper T subsets (TFH), follicular regulatory T cells (TFR), and B lymphocyte subpopulations, reflecting the ongoing germinal center reactions in SLE patients. Peripheral blood samples were obtained from ten SLE patients before the initiation of anifrolumab treatment, and at months 6 and 12 of the intervention period. Flow cytometry analysis was performed to assess the frequencies of circulating TFH cell subsets, TFR cells, and certain B cell subpopulations. Serological parameters, including autoantibody levels and complement components, were determined as part of the routine diagnostic evaluation. We observed a significant and sustained reduction in the percentage of activated circulating TFH cells. Notably, the frequency of CXCR3?CCR6+ TFH17 cells decreased, whereas the proportion of CXCR3+CCR6? TFH1 cells increased significantly. Furthermore, the proportion of the IgD?CD27? double-negative B lymphocytes was also significantly reduced. These findings suggest that anifrolumab therapy attenuates TFH cell activation, which may contribute to its clinical efficacy by modulating germinal center responses in SLE.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
systemic lupus erythematosus
anifrolumab
follicular helper T cells
Megjelenés:International Journal Of Molecular Sciences. - 26 : 15 (2025), p. 1-10. -
További szerzők:Gyetvai Ágnes (1978-) (biotechnológus) Papp Gábor (1984-) (belgyógyász) Tarr Tünde (1976-) (belgyógyász, allergológus és klinikai immunológus)
Pályázati támogatás:124177
OTKA
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2.

001-es BibID:BIBFORM100414
035-os BibID:(scopus)85125084009 (wos)000772754000001
Első szerző:Diós Ádám (molekuláris biológus)
Cím:Changes in Non-deamidated versus Deamidated Epitope Targeting and Disease Prediction during the Antibody Response to Gliadin and Transglutaminase of Infants at Risk for Celiac Disease / Ádám Diós, Bharani Srinivasan, Judit Gyimesi, Katharina Werkstetter, Rudolf Valenta, Sibylle Koletzko, Ilma R. Korponay-Szabó
Dátum:2022
ISSN:1661-6596 1422-0067
Megjegyzések:Celiac disease (CeD) is a conditional autoimmune disorder with T-cell mediated immune response to gluten coupled with antibody production to gliadin and the self-protein tissue transglutaminase (TG2). TG2 contributes to CeD pathomechanism by deamidating gliadin, thereby generating more immunogenic peptides. Anti-gliadin antibodies may appear before the autoantibody production. The scope of this study was to dissect these early antibody responses by investigating serum sam-ples collected during the PreventCD prospective double-blind study (www.preventcd.com), where infants with high CeD risk were randomized to 200 mg daily gluten intake or to placebo from 4 to 6 months of age, then followed by frequent blood testing on regular gluten consumption in both groups. After primary gluten intake, children with or without later CeD produced IgA and IgG antibodies which preferentially recognized non-deamidated gliadin peptides. At CeD development with anti-TG2 seroconversion, there was a significant increase in the antibody reac-tion toward deamidated gliadin peptides (DGP) with maturation in the binding strength for the PEQPFP gamma-gliadin core peptide. The earliest produced autoantibodies targeted TG2's celiac epitope 2. Our results reveal a qualitative change in the gliadin-directed humoral immune re-sponse at the time when anti-TG2 antibodies appear, but anti-DGP antibodies in the absence of anti-TG2 antibodies are not disease-predictive.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
celiac disease
deamidated gliadin peptides
transglutaminase antibody
Megjelenés:International Journal Of Molecular Sciences. - 23 : 5 (2022), p. 1-16. -
További szerzők:Srinivasan, Bharani Gyimesi Judit Werkstetter, Katharina (gyermekgyógyász, gasztroenterológus) Valenta, Rudolf Koletzko, Sibylle Korponay-Szabó Ilma (1959-) (gyermekgyógyász)
Pályázati támogatás:NKFIH 120392
OTKA
EFOP-3.6.1-16-2016-00022
EFOP
DTP3-571-1.2
Egyéb
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
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