TY - JOUR
AU - Gémes, Nikolett
AU - Rónaszéki, Benedek
AU - Modok, Szabolcs
AU - Borbényi, Zita
AU - Földesi, Imre
AU - Trucza, Éva Gabriella
AU - Godza, Blanka
AU - László, Zsuzsanna
AU - Csernus, Balázs
AU - Krenács, László
AU - Bagdi, Enikő
AU - Szabó, Enikő
AU - Puskás, László
AU - Bertagnolo, Valeria
AU - Szebeni, Gábor
TI - Multiplex immunophenotyping of human acute myeloid leukemia patients revealed single -cell heterogeneity with special attention on therapy sensitive and therapy resistant subpopulations
JF - FRONTIERS IN IMMUNOLOGY
J2 - FRONT IMMUNOL
VL - 16
PY - 2025
PG - 14
SN - 1664-3224
DO - 10.3389/fimmu.2025.1563386
UR - https://m2.mtmt.hu/api/publication/36099827
ID - 36099827
N1 - Funding Agency and Grant Number: National Research, Development, and Innovation Office (NKFI), Hungary [2023-1.1.1-PIACI_FOKUSZ-2024-00036, 2020-1.1.6-JOVO- 2021-00003, 2022-1.2.6-TET-IPARI-TR-2022-00023, 142877 FK22]; KDP-2021 Program for NG of the Ministry for Innovation and Technology from the source of the National Research, Development and Innovation Fund [C1764415]; Janos Bolyai Research Scholarship of the Hungarian Academy of Sciences [BO/00582/22/8]
Funding text: The author(s) declare that financial support was received for the research and/or publication of this article. This research was funded by the 2023-1.1.1-PIACI_FOKUSZ-2024-00036, 2020-1.1.6-JOVO- 2021-00003, 2022-1.2.6-TET-IPARI-TR-2022-00023 and 142877 FK22, grant from the National Research, Development, and Innovation Office (NKFI), Hungary. This work was supported by the KDP-2021 Program for NG (C1764415) of the Ministry for Innovation and Technology from the source of the National Research, Development and Innovation Fund. This work was supported by the Janos Bolyai Research Scholarship of the Hungarian Academy of Sciences BO/00582/22/8 (GJS).
LA - English
DB - MTMT
ER -
TY - JOUR
AU - Balog, Attila
AU - Kari, Beáta
AU - Kotogány, Edit
AU - Gémes, Nikolett
AU - Honfi, Dániel György
AU - Cselei, N.
AU - Szebeni, Gábor
TI - Multiplex immunophenotyping of petients with antiphospholipid syndrome or seropositivity without clinical symptomes
JF - ANNALS OF THE RHEUMATIC DISEASES
J2 - ANN RHEUM DIS
VL - 84
PY - 2025
IS - Suppl 1
SP - 1543
EP - 1543
PG - 1
SN - 0003-4967
DO - 10.1016/j.ard.2025.06.911
UR - https://m2.mtmt.hu/api/publication/36235342
ID - 36235342
N1 - Supplement: 1
WoS:hiba:001525073100037 2025-12-29 11:00 DOI azonosító nem egyezik
LA - English
DB - MTMT
ER -
TY - JOUR
AU - Novák, Ádám
AU - Zajta, Erik
AU - Csikós, Máté Lajos
AU - Halmos, Emese
AU - Horváth, Márton
AU - Tildy, Orsolya
AU - Szekeres, András
AU - Svorenj, Gergő
AU - Gémes, Nikolett
AU - Szebeni, Gábor
AU - Tóth, Renáta
AU - Gácser, Attila
TI - Comprehensive analysis of human keratinocyte interactions with Candida albicans and Candida parapsilosis
JF - VIRULENCE
J2 - VIRULENCE
VL - 16
PY - 2025
IS - 1
PG - 20
SN - 2150-5594
DO - 10.1080/21505594.2025.2532815
UR - https://m2.mtmt.hu/api/publication/36264592
ID - 36264592
N1 - Funding Agency and Grant Number: EU's Horizon 2020 research and innovation program [739593]; HUN-REN [2001007]; Hungarian Scientific Research Fund NKFIH [K147510]; Centre of Excellence for Interdisciplinary Research, Development and Innovation of the University of Szeged, Competence Centre for Molecular Biology, Bionics and Biotechnology; Louis-Jeantet Foundation; Hungarian Academy of Sciences [BO/00351/23/8, BO/00582/22/8]; National Research, Development and Innovation Office (NKFIH) [PD 138450]; National Research, Development, and Innovation Office; National Academy of Scientist Education Program of the National Biomedical Foundation; [2023-1.1.1-PIACI_FKUSZ-2024-00036]; [FK22-142877]
Funding text: The project was supported by EU's Horizon 2020 research and innovation program under grant agreement No. [739593], by the grant HUN-REN [2001007], by the Hungarian Scientific Research Fund NKFIH [K147510] and the Centre of Excellence for Interdisciplinary Research, Development and Innovation of the University of Szeged, Competence Centre for Molecular Biology, Bionics and Biotechnology. The research was also supported by the Louis-Jeantet Foundation. RT was supported by the Janos Bolyai Research Scholarship of the Hungarian Academy of Sciences, BO/00351/23/8. R.T.was financed by the National Research, Development and Innovation Office (NKFIH) through grant no. [PD 138450]. This research was funded by the 2023-1.1.1-PIACI_F & Oacute;KUSZ-2024-00036 (NKFIH), [FK22-142877] (GS), grant from the National Research, Development, and Innovation Office. This work was supported by the Janos Bolyai Research Scholarship of the Hungarian Academy of Sciences BO/00582/22/8 (GS). This research work and G.S. was supported by the National Academy of Scientist Education Program of the National Biomedical Foundation under the sponsorship of the Hungarian Ministry of Culture and Innovation.
LA - English
DB - MTMT
ER -
TY - JOUR
AU - Nógrádi, Bernát
AU - Molnár, Kinga
AU - Kristóf, Rebeka
AU - Horváth, Orsolya
AU - Huang, Yu-Ting
AU - Ridgway, Zara
AU - Elicegui, Amaia
AU - Fuertes-Alvarez, Sandra
AU - Alonso-Martin, Sonia
AU - Szebeni, Gábor
AU - Gémes, Nikolett
AU - Ramadan, Abdullah
AU - Smith, Hannah L.
AU - Krizbai, István Adorján
AU - Patai, Roland
AU - Siklós, László
AU - Klivényi, Péter
AU - Chaytow, Helena
AU - Gillingwater, Thomas H.
TI - The CCL2-CCR2 axis drives neuromuscular denervation in amyotrophic lateral sclerosis
JF - NATURE COMMUNICATIONS
J2 - NAT COMMUN
VL - 16
PY - 2025
IS - 1
PG - 16
SN - 2041-1723
DO - 10.1038/s41467-025-62351-3
UR - https://m2.mtmt.hu/api/publication/36280462
ID - 36280462
N1 - Funding Agency and Grant Number: Instituto de Salud Carlos III (ISCIII); European Union [PI22/00433]; ISCIII Programa Fortalece del Ministerio de Ciencia e Innovacion [FORT23/00026]; Department of Education of the Basque Country through the IKUR strategy; Osasun Saila, Eusko Jaurlaritzako [2020111032, 2023111035]; National Research, Development, and Innovation Office [FK-143326]; Ministry of Culture and Innovation of Hungary and the National Research, Development and Innovation Fund [TKP2021-EGA-32]; My Name'5 Doddie Foundation [DOD/14/32]; MND Scotland [2021/MNDS/RP/8430GILL]; Department of Education of the Basque Country [R-3825]; LifeArc; Spanish Health Institute Carlos III; Research Training Fellowship of the European Academy of Neurology; Gipuzkoa Fellow of Talent Attraction and Retention; Hungarian Eoetvoes Fellowship of the Government of Hungary; Postdoctoral Research Grant of the Albert Szent-Gyoergyi Medical School, University of Szeged; Janos Bolyai Research Scholarship of the Hungarian Academy of Sciences [BO/00582/22/8]; New National Excellence Program of the Ministry for Innovation and Technology [UNKP-23-5-SZTE-694]; [PRE_2020_1_0119]; [CD21/00066]; [2019-FELL-000010-01]
Funding text: The authors would like to thank all patients who contributed to this study. They would also like to thank support staff in the IMPACT microscopy facility and the Biological Research Resources facility at the University of Edinburgh. The authors also acknowledge the microscopy support of the Cellular Imaging Laboratory at the BRC HUN-REN Core Facility and the FCBI Advanced Core Facility of Hungarian Centre of Excellence for Molecular Medicine (HCEMM). The authors would like to thank the following funders for support of the project: Instituto de Salud Carlos III (ISCIII) and the European Union (SA-M, project PI22/00433), ISCIII Programa Fortalece del Ministerio de Ciencia e Innovacion (SA-M, project FORT23/00026), Department of Education of the Basque Country through the IKUR strategy (SA-M, NEURODEGENPROT), Osasun Saila, Eusko Jaurlaritzako (SA-M, projects 2020111032, 2023111035), National Research, Development, and Innovation Office (RP, project FK-143326), TKP2021-EGA funding scheme by the Ministry of Culture and Innovation of Hungary and the National Research, Development and Innovation Fund (PK, project TKP2021-EGA-32), My Name'5 Doddie Foundation (THG and HC, project DOD/14/32), MND Scotland (THG and HC, project 2021/MNDS/RP/8430GILL), LifeArc (THG and HC, project R-3825), Research Training Fellowship of the European Academy of Neurology (BN), Hungarian Eoetvoes Fellowship of the Government of Hungary (BN), Postdoctoral Research Grant of the Albert Szent-Gyoergyi Medical School, University of Szeged (BN), Janos Bolyai Research Scholarship of the Hungarian Academy of Sciences, (GJS, project BO/00582/22/8), New National Excellence Program of the Ministry for Innovation and Technology (GJS, project UNKP-23-5-SZTE-694), Department of Education of the Basque Country (AE, PhD fellowship PRE_2020_1_0119), Sara Borrell contract from the Spanish Health Institute Carlos III (SF-A, project CD21/00066), Gipuzkoa Fellow of Talent Attraction and Retention (SA-M, project 2019-FELL-000010-01).
LA - English
DB - MTMT
ER -
TY - JOUR
AU - Várnai, Réka
AU - Szebeni, Gábor
AU - Gémes, Nikolett
AU - Schwarcz, Attila
AU - Molnár, Tihamér
AU - Oláh, Csaba Zsolt
AU - Csécsei, Péter
TI - Immune Checkpoint Dysregulation in Aneurysmal Subarachnoid Hemorrhage: A Prospective Study of sCTLA-4 and sPD-L1 as Biomarkers of Symptomatic Vasospasm
JF - INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
J2 - INT J MOL SCI
VL - 26
PY - 2025
IS - 17
PG - 15
SN - 1661-6596
DO - 10.3390/ijms26178228
UR - https://m2.mtmt.hu/api/publication/36298925
ID - 36298925
N1 - Funding Agency and Grant Number: Hungarian NRDI Fund [NKFI-FK-146159]; National Laboratory for Translational Neuroscience project [RRF-2.3.1-21-2022-00011]; National Research, Development, and Innovation Office (NKFI), Hungary [2023-1.1.1-PIACI_FOKUSZ-2024-00036, 2022-1.2.6-TEET-IPARI-TR-2022-00023, 142877 FK22]; SZAOK-SZBK Collaboration grant [IV-134-62-1/2024.SZAOK]; Janos Bolyai Research Scholarship of the Hungarian Academy of Sciences [BO/00582/22/8]; University of Pecs [015_2024_PTE_RK/12]
Funding text: This work was supported by the Hungarian NRDI Fund (NKFI-FK-146159) and the National Laboratory for Translational Neuroscience project (RRF-2.3.1-21-2022-00011). This research was also funded by the 2023-1.1.1-PIACI_FOKUSZ-2024-00036, 2022-1.2.6-TEET-IPARI-TR-2022-00023, and 142877 FK22, grants from the National Research, Development, and Innovation Office (NKFI), Hungary. This work was supported by the SZAOK-SZBK Collaboration grant (IV-134-62-1/2024.SZAOK) and the Janos Bolyai Research Scholarship of the Hungarian Academy of Sciences BO/00582/22/8 (GJS). The work was also supported by the 015_2024_PTE_RK/12 grant from the University of Pecs (RV).
AB - Aneurysmal subarachnoid hemorrhage (aSAH) is a severe stroke subtype often complicated by symptomatic cerebral vasospasm (sVP), contributing to delayed cerebral ischemia and poor outcomes. Immune dysregulation, particularly T-cell imbalances and pro-inflammatory cytokines, is implicated in vasospasm development. Soluble immune checkpoint proteins—CTLA-4 (sCTLA-4) and PD-L1 (sPD-L1)—regulate immune homeostasis and may serve as biomarkers or modulators of inflammation in aSAH. This prospective cohort study included 179 aSAH patients, divided into sVP+ (n = 48) and sVP− (n = 131), plus 50 healthy controls. Serum sCTLA-4 and sPD-L1 levels were measured on days 1, 5, and 9 post-ictus using Luminex xMAP. Associations with clinical outcomes were analyzed using non-parametric statistics and hierarchical clustering. Both sCTLA-4 and sPD-L1 were significantly elevated in sVP+ patients versus sVP− and controls, increasing over time. sCTLA-4 was significantly higher in sVP+ on days 5 (p = 0.001) and 9 (p < 0.001), and sPD-L1 on days 5 and 9 (both p < 0.001). Clustering revealed distinct expression patterns between sVP+ and sVP− groups. Elevated sCTLA-4 and sPD-L1 levels are associated with sVP after aSAH and may serve as biomarkers for early immune dysfunction, offering insights into potential therapeutic targets.
LA - English
DB - MTMT
ER -
TY - JOUR
AU - Lenzsér, Gábor
AU - Szebeni, Gábor
AU - Balogh, Fanni
AU - Gémes, Nikolett
AU - Schwarcz, Attila
AU - Csécsei, Péter
TI - Claudin proteins and hemorrhage severity in aneurysmal subarachnoid hemorrhage: Correlation with modified Fisher score but not functional outcome
JF - NEUROSURGICAL REVIEW
J2 - NEUROSURG REV
VL - 48
PY - 2025
IS - 1
PG - 10
SN - 0344-5607
DO - 10.1007/s10143-025-03829-y
UR - https://m2.mtmt.hu/api/publication/36389897
ID - 36389897
N1 - Funding Agency and Grant Number: University of Pcs
Funding text: We gratefully acknowledge the patients and their families for their generous contribution of serum samples, which made this study possible. We also thank the clinical staff involved in the collection and processing of samples for their invaluable support. Their collaboration was essential to the success of this research.
AB - Background: Aneurysmal subarachnoid hemorrhage (aSAH) is a critical condition characterized by blood-brain barrier (BBB) disruption. Tight junction proteins, claudin-3 (CLDN3) and claudin-5 (CLDN5), are key regulators of BBB integrity and may serve as biomarkers of hemorrhage severity. Methods: In this prospective cohort study, 200 patients with aSAH were evaluated. Serum CLDN3 and CLDN5 levels were measured on days 1, 5, and 9 post-ictus and compared with healthy and aneurysm-bearing controls. Patients were stratified by modified Fisher Score (mFS), World Federation of Neurosurgical Societies (WFNS) score, and 3-month modified Rankin Scale (mRS). Associations with complications, including delayed cerebral ischemia (DCI) and infection, were also assessed. Results: CLDN3 and CLDN5 levels were significantly elevated in aSAH patients compared to controls ( p <0.01 and p <0.0001, respectively), with CLDN5 levels consistently higher than CLDN3 at all time points ( p <0.0001). CLDN5 levels were consistently higher than CLDN3 at all measured time points, and neither CLDN3 nor CLDN5 showed significant temporal variation between days 1, 5, and 9. Both markers showed significant positive correlation with mFS, with higher levels observed in mFS3 and mFS4 groups ( p <0.05 to p <0.0001). No association was found between CLDN3 and 5 levels and WFNS score, 3-month mRS, age, sex, comorbidities, inflammatory markers, or DCI. Conclusion: Elevated serum CLDN3 and especially CLDN5 levels reflect hemorrhage extent and potential BBB disruption in aSAH. Their strong correlation with mFS suggests utility in grading imageological hemorrhagic severity, though not in predicting long-term functional outcomes. CLDN5 emerges as a promising biomarker for early assessment of BBB integrity in neurovascular injury.
LA - English
DB - MTMT
ER -
TY - JOUR
AU - Szebeni, Gábor
AU - Gémes, Nikolett
AU - Neuperger, Patricia
AU - Szabó, Enikő
AU - Balog, József Ágoston
AU - Honfi, Dániel György
AU - Balog, Attila
AU - Toldi, Gergely
TI - The effect of baricitinib on pSTAT3 levels in IL-6- or IL-15-stimulated PBMCs isolated from patients with SLE
JF - FRONTIERS IN IMMUNOLOGY
J2 - FRONT IMMUNOL
VL - 16
PY - 2025
PG - 11
SN - 1664-3224
DO - 10.3389/fimmu.2025.1675350
UR - https://m2.mtmt.hu/api/publication/36391088
ID - 36391088
N1 - Funding Agency and Grant Number: National Research, Development, and Innovation Office (NKFI), Hungary [2023-1.1.1-PIACI_FOKUSZ-2024-00036, 142877 FK22]; University of Szeged [IV-134-62-1/2024.SZAOK]; Hungarian Academy of Sciences [BO/00582/22/8]; University of Szeged Open Access Fund [BO/00582/22/8]
Funding text: The author(s) declare financial support was received for the research and/or publication of this article. This research was funded by the 2023-1.1.1-PIACI_FOKUSZ-2024-00036 and 142877 FK22 grants from the National Research, Development, and Innovation Office (NKFI), Hungary. This work was supported by the IV-134-62-1/2024.SZAOK, SZAOK-SZBK collaboration grant of the University of Szeged; the Janos Bolyai Research Scholarship of the Hungarian Academy of Sciences BO/00582/22/8 (GS); and the University of Szeged Open Access Fund (GS).
LA - English
DB - MTMT
ER -
TY - JOUR
AU - Abdallah, Hiba Faroug Muddather
AU - Nasibova, Tohfa
AU - Szebeni, Gábor
AU - Gémes, Nikolett
AU - Bózsity-Faragó, Noémi
AU - Minorics, Renáta
AU - Garayev, Eldar
AU - Orhan, Ilkay Erdogan
AU - Herbette, Gaëtan
AU - Schelz, Zsuzsanna
AU - Hohmann, Judit
AU - Zupkó, István
TI - Potential anticancer effects of Peganum harmala in human papillomavirus-related cervical and head and neck cancer cells
JF - FRONTIERS IN PHARMACOLOGY
J2 - FRONT PHARMACOL
VL - 16
PY - 2025
PG - 19
SN - 1663-9812
DO - 10.3389/fphar.2025.1668827
UR - https://m2.mtmt.hu/api/publication/36444224
ID - 36444224
LA - English
DB - MTMT
ER -
TY - JOUR
AU - Balogh, Gergő Mihály
AU - Koncz, Balázs
AU - Asztalos, Leó
AU - Ari, Eszter
AU - Gémes, Nikolett
AU - Szebeni, Gábor
AU - Papp, Benjamin Tamás
AU - Tóth, Franciska
AU - Papp, Balázs
AU - Pál, Csaba
AU - Manczinger, Máté
TI - C > U mutations generate immunogenic peptides in SARS-CoV-2
JF - NATURE COMMUNICATIONS
J2 - NAT COMMUN
VL - 16
PY - 2025
IS - 1
PG - 13
SN - 2041-1723
DO - 10.1038/s41467-025-65251-8
UR - https://m2.mtmt.hu/api/publication/36444923
ID - 36444923
N1 - Funding Agency and Grant Number: European Union [739593]; European Union's Horizon Europe research and innovation program [101136582]; European Research Council [ERC-2023-ADG 101142626]; National Research Development and Innovation Office [K 146323, 2022-2.1.1-NL-2022-00008, FK-142312, PD-146654, FK22-142877, 2023-1.1.1-PIACI_FOKUSZ-2024-00036]; National Research, Development, and Innovation Office (NKFI), Hungary; National Academy of Scientist Education; Hungarian Ministry of Innovation and Technology [FEIF/646-4/2021-ITM_SZERZ, TKCS-2024/66, RRF-2.3.1-21-2022-00006, NKP-22-4, NKP-23-4, NKP-23-5]; New National Excellence Program of the Ministry for Culture and Innovation from the source of the National Research, Development and Innovation Fund [C1764415]; Ministry for Innovation and Technology from the source of the National Research, Development and Innovation Fund; Bolyai Jnos Research Fellowship [BO/00582/22/8]; Hungarian Academy of Sciences [44917]
Funding text: The work was supported by the European Union's Horizon 2020 research and innovation program grant No. 739593 (M.M., B.K, G.M.B, and B.P); the European Union's Horizon Europe research and innovation program under grant agreement No 101136582 Acronym ID-DarkMatter-NCD (M.M.); the European Research Council ERC-2023-ADG 101142626 FutureAntibiotics (C.P.); the National Research Development and Innovation Office K 146323 (C.P.); the National Laboratory of Biotechnology Grant 2022-2.1.1-NL-2022-00008 (C.P.); the Hungarian Scientific Research Fund grant FK-142312 (M.M.), PD-146654 (B.K.), FK22-142877 (G.J.S.) and 2023-1.1.1-PIACI_FOKUSZ-2024-00036 (G.J.S.) from the National Research, Development, and Innovation Office (NKFI), Hungary; the National Academy of Scientist Education under the sponsorship of the Hungarian Ministry of Innovation and Technology (FEIF/646-4/2021-ITM_SZERZ), the HUN-REN (TKCS-2024/66; to B.P. and E.A.) and the National Laboratory for Health Security grant RRF-2.3.1-21-2022-00006 (B.P.). G.M.B. was supported by the UNKP-22-4 and UNKP-23-4, M.M., B.K., and G.J.S. were supported by the UNKP-23-5 New National Excellence Program of the Ministry for Culture and Innovation from the source of the National Research, Development and Innovation Fund. N.G. was supported by the KDP-2021 Program (C1764415) of the Ministry for Innovation and Technology from the source of the National Research, Development and Innovation Fund. M.M., B.K. and G.J.S. were supported by the Bolyai Janos Research Fellowship (BO/00582/22/8) of the Hungarian Academy of Sciences. COVID-19 outcome analysis was performed using data from the UK Biobank Resource under application number 44917.
AB - The rapid spread of SARS-CoV-2 worldwide has given rise to numerous variants. While the impact of viral mutations on antibody escape has been extensively studied, an unresolved issue concerns how emerging mutations shape HLA-restricted T-cell immune responses. Here, we analyse SARS-CoV-2 genomic variants, showing that 27% of the mutations are C > U transitions, a phenomenon common in human RNA viruses and primarily attributed to APOBEC3 enzyme-driven mutagenesis. We find that this mutation bias generally enhances viral peptide binding to human leukocyte antigen class I (HLA-I) molecules, producing immunogenic epitopes that trigger cytotoxic adaptive immune responses in most individuals across diverse populations. We also identify several HLA-I variants that are especially well-suited for presenting viral epitopes generated by these mutations. Intriguingly, individuals carrying these specific alleles are predominantly located in South and East Asia. Finally, we show that carrying HLA-I molecules that are less likely to bind C > U-induced viral peptides increases risk for severe COVID-19 disease. Our work suggests a link between C > U hypermutation and HLA-I-based presentation of viral epitopes, which may reflect the evolutionary outcome of ancient RNA virus pandemics. More broadly, our findings imply that SARS-CoV-2 diversification leads to ongoing gains of T-cell epitopes despite natural selection favouring immune escape.
LA - English
DB - MTMT
ER -
TY - JOUR
AU - Szabó, Enikő
AU - Faragó, Anna
AU - Bodor, Gergely
AU - Gémes, Nikolett
AU - Puskás, László
AU - Kovács, László
AU - Szebeni, Gábor
TI - Identification of immune subsets with distinct lectin binding signatures using multi-parameter flow cytometry: correlations with disease activity in systemic lupus erythematosus
JF - FRONTIERS IN IMMUNOLOGY
J2 - FRONT IMMUNOL
VL - 15
PY - 2024
PG - 22
SN - 1664-3224
DO - 10.3389/fimmu.2024.1380481
UR - https://m2.mtmt.hu/api/publication/34840255
ID - 34840255
N1 - Funding Agency and Grant Number: Nemzeti Kutatsi Fejlesztsi s Innovcis Hivatal10.13039/501100011019
Funding text: No Statement Available
A közlemény a Bolyai János Kutatási Ösztöndíj (BO/00582/22/8) segítségével jött létre.
AB - Cell surface glycosylation can influence protein-protein interactions with particular relevance to changes in core fucosylation and terminal sialylation. Glycans are ligands for immune regulatory lectin families like galectins (Gals) or sialic acid immunoglobulin-like lectins (Siglecs). This study delves into the glycan alterations within immune subsets of systemic lupus erythematosus (SLE).MethodsEvaluation of binding affinities of Galectin-1, Galectin-3, Siglec-1, Aleuria aurantia lectin (AAL, recognizing core fucosylation), and Sambucus nigra agglutinin (SNA, specific for α-2,6-sialylation) was conducted on various immune subsets in peripheral blood mononuclear cells (PBMCs) from control and SLE subjects. Lectin binding was measured by multi-parameter flow cytometry in 18 manually gated subsets of T-cells, NK-cells, NKT-cells, B-cells, and monocytes in unstimulated resting state and also after 3-day activation. Stimulated pre-gated populations were subsequently clustered by FlowSOM algorithm based on lectin binding and activation markers, CD25 or HLA-DR.ResultsElevated AAL, SNA and CD25+/CD25- SNA binding ratio in certain stimulated SLE T-cell subsets correlated with SLE Disease Activity Index 2000 (SLEDAI-2K) scores. The significantly increased frequencies of activated AALlow Siglec-1low NK metaclusters in SLE also correlated with SLEDAI-2K indices. In SLE, activated double negative NKTs displayed significantly lower core fucosylation and CD25+/CD25- Siglec-1 binding ratio, negatively correlating with disease activity. The significantly enhanced AAL binding in resting SLE plasmablasts positively correlated with SLEDAI-2K scores.ConclusionAlterations in the glycosylation of immune cells in SLE correlate with disease severity, which might represent potential implications in the pathogenesis of SLE.
LA - English
DB - MTMT
ER -