@article{MTMT:34656799,
	title = {Molecular characterisation of lupus low disease activity state (LLDAS) and DORIS remission by whole-blood transcriptome-based pathways in a pan-European systemic lupus erythematosus cohort},
	url = {https://m2.mtmt.hu/api/publication/34656799},
	author = {Parodis, Ioannis and Lindblom, Julius and Barturen, Guillermo and Ortega-Castro, Rafaela and Cervera, Ricard and Pers, Jacques-Olivier and Genre, Fernanda and Hiepe, Falk and Gerosa, Maria and Kovács, László and De Langhe, Ellen and Piantoni, Silvia and Stummvoll, Georg and Vasconcelos, Carlos and Vigone, Barbara and Witte, Torsten and Alarcón-Riquelme, Marta E and Beretta, Lorenzo},
	doi = {10.1136/ard-2023-224795},
	journal-iso = {ANN RHEUM DIS},
	journal = {ANNALS OF THE RHEUMATIC DISEASES},
	unique-id = {34656799},
	issn = {0003-4967},
	abstract = {To unveil biological milieus underlying low disease activity (LDA) and remission versus active systemic lupus erythematosus (SLE).We determined differentially expressed pathways (DEPs) in SLE patients from the PRECISESADS project (NTC02890121) stratified into patients fulfilling and not fulfilling the criteria of (1) Lupus LDA State (LLDAS), (2) Definitions of Remission in SLE remission, and (3) LLDAS exclusive of remission.We analysed data from 321 patients; 40.8% were in LLDAS, and 17.4% in DORIS remission. After exclusion of patients in remission, 28.3% were in LLDAS. Overall, 604 pathways differed significantly in LLDAS versus non-LLDAS patients with an false-discovery rate-corrected p (q)<0.05 and a robust effect size (dr)≥0.36. Accordingly, 288 pathways differed significantly between DORIS remitters and non-remitters (q<0.05 and dr≥0.36). DEPs yielded distinct molecular clusters characterised by differential serological, musculoskeletal, and renal activity. Analysis of partially overlapping samples showed no DEPs between LLDAS and DORIS remission. Drug repurposing potentiality for treating SLE was unveiled, as were important pathways underlying active SLE whose modulation could aid attainment of LLDAS/remission, including toll-like receptor (TLR) cascades, Bruton tyrosine kinase (BTK) activity, the cytotoxic T lymphocyte antigen 4 (CTLA-4)-related inhibitory signalling, and the nucleotide-binding oligomerization domain leucine-rich repeat-containing protein 3 (NLRP3) inflammasome pathway.We demonstrated for the first time molecular signalling pathways distinguishing LLDAS/remission from active SLE. LLDAS/remission was associated with reversal of biological processes related to SLE pathogenesis and specific clinical manifestations. DEP clustering by remission better grouped patients compared with LLDAS, substantiating remission as the ultimate treatment goal in SLE; however, the lack of substantial pathway differentiation between the two states justifies LLDAS as an acceptable goal from a biological perspective.},
	keywords = {Autoimmune Diseases; Autoimmunity; Lupus Erythematosus, Systemic; Immune System Diseases; Outcome Assessment, Health Care},
	year = {2024},
	eissn = {1468-2060},
	orcid-numbers = {Kovács, László/0000-0003-4457-1430}
}

@article{MTMT:34149961,
	title = {Differenciáldiagnosztikai kihívás nyelőcső motilitási zavar kapcsán},
	url = {https://m2.mtmt.hu/api/publication/34149961},
	author = {Ladóczky-Hulló, Daniella and Bocskai, Márta and Kovács, László},
	journal-iso = {MAGYAR REUMATOL},
	journal = {MAGYAR REUMATOLÓGIA},
	volume = {64},
	unique-id = {34149961},
	issn = {0139-4495},
	year = {2023},
	pages = {172-173},
	orcid-numbers = {Kovács, László/0000-0003-4457-1430}
}

@article{MTMT:34110982,
	title = {Complement component C4 structural variation and quantitative traits contribute to sex-biased vulnerability in systemic sclerosis},
	url = {https://m2.mtmt.hu/api/publication/34110982},
	author = {Kerick, Martin and Acosta-Herrera, Marialbert and Simeón-Aznar, Carmen Pilar and Callejas, José Luis and Assassi, Shervin and Proudman, Susanna M and Nikpour, Mandana and Hunzelmann, Nicolas and Moroncini, Gianluca and de Vries-Bouwstra, Jeska K and Orozco, Gisela and Barton, Anne and Herrick, Ariane L and Terao, Chikashi and Allanore, Yannick and Fonseca, Carmen and Alarcón-Riquelme, Marta Eugenia and Radstake, Timothy R D J and Beretta, Lorenzo and Denton, Christopher P and Mayes, Maureen D and Martin, Javier},
	doi = {10.1038/s41525-022-00327-8},
	journal-iso = {NPJ GENOM MED},
	journal = {NPJ GENOMIC MEDICINE},
	volume = {7},
	unique-id = {34110982},
	issn = {2056-7944},
	abstract = {Copy number (CN) polymorphisms of complement C4 play distinct roles in many conditions, including immune-mediated diseases. We investigated the association of C4 CN with systemic sclerosis (SSc) risk. Imputed total C4, C4A, C4B, and HERV-K CN were analyzed in 26,633 individuals and validated in an independent cohort. Our results showed that higher C4 CN confers protection to SSc, and deviations from CN parity of C4A and C4B augmented risk. The protection contributed per copy of C4A and C4B differed by sex. Stronger protection was afforded by C4A in men and by C4B in women. C4 CN correlated well with its gene expression and serum protein levels, and less C4 was detected for both in SSc patients. Conditioned analysis suggests that C4 genetics strongly contributes to the SSc association within the major histocompatibility complex locus and highlights classical alleles and amino acid variants of HLA-DRB1 and HLA-DPB1 as C4-independent signals.},
	year = {2022},
	eissn = {2056-7944},
	orcid-numbers = {Kovács, László/0000-0003-4457-1430}
}

@book{MTMT:33138272,
	title = {Reumatológia - Egyetemi jegyzet Reumatológia tantárgyhoz. ETSZK Gyógytornász (BSc) szakirány 2022},
	url = {https://m2.mtmt.hu/api/publication/33138272},
	isbn = {9789633068878},
	author = {Kovács, László and Burcsár, Szilárd and Dobi, Diána and Balog, Attila and Ladóczky-Hulló, Daniella and Honfi, Dániel György and Bocskai, Márta and Kádár, Gabriella and Sümegi, Viktória and Varga, Borisz and Hemelein, Rita Adrienn and Besenyi, Zsuzsanna and Legány, Nóra},
	editor = {Kovács, László},
	publisher = {SZTE, Szent-Györgyi Albert Klinikai Központ, Reumatológiai és Immunológiai Klinika},
	unique-id = {33138272},
	year = {2022},
	orcid-numbers = {Kovács, László/0000-0003-4457-1430; Besenyi, Zsuzsanna/0000-0001-9115-9620; Kovács, László/0000-0003-4457-1430}
}

@article{MTMT:32869486,
	title = {Machine learning identifies a common signature for anti-SSA/Ro60 antibody expression across autoimmune diseases},
	url = {https://m2.mtmt.hu/api/publication/32869486},
	author = {Foulquier, Nathan and Le Dantec, Christelle and Bettacchioli, Eleonore and Jamin, Christophe and Alarcón-Riquelme, Marta E and Pers, Jacques-Olivier},
	doi = {10.1002/art.42243},
	journal-iso = {ARTHRITIS RHEUMATOL},
	journal = {ARTHRITIS & RHEUMATOLOGY},
	volume = {74},
	unique-id = {32869486},
	issn = {2326-5191},
	abstract = {Anti-Ro autoantibodies are among the most frequently detected extractable nuclear antigen autoantibodies, mainly associated with primary Sjögren's syndrome (pSS), systemic lupus erythematosus (SLE) and undifferentiated connective tissue disease (UCTD). Is there a common signature to all patients expressing anti-Ro60 autoantibodies regardless of their disease phenotype?Using high-throughput multi-omics data collected within the cross-sectional cohort from the PRECISESADS IMI project (genetic, epigenomic, transcriptomic, combined with flow cytometric data, multiplexed cytokines, classical serology and clinical data), we assessed by machine learning the integrated molecular profiling of 520 anti-Ro60-positive (anti-Ro60+ ) compared to 511 anti-Ro60-negative (anti-Ro60- ) patients with pSS, SLE and UCTD, and 279 healthy controls (HCs).The selected features for RNA-Seq, DNA methylation and GWAS data allowed a clear separation between anti-Ro60+ and anti-Ro60- patients. The different features selected by machine learning from the anti-Ro60+ patients constitute specific signatures when compared to anti-Ro60- patients and HCs. Remarkably, the transcript z-score of three genes (ATP10A, MX1 and PARP14), presenting an overexpression associated with a hypomethylation and genetic variation, and independently identified by the Boruta algorithm, was clearly higher in anti-Ro60+ patients compared to anti-Ro60- patients in all the diseases. We demonstrate that these signatures, enriched in interferon stimulated genes, were also found in anti-Ro60+ patients with rheumatoid arthritis and systemic sclerosis and remained stable over time and not influenced by treatment.Anti-Ro60+ patients present a specific inflammatory signature regardless of their disease suggesting that a dual therapeutic approach targeting both Ro-associated RNAs and anti-Ro60 autoantibodies should be considered.},
	year = {2022},
	eissn = {2326-5205},
	pages = {1706-1719},
	orcid-numbers = {Kovács, László/0000-0003-4457-1430}
}

@book{MTMT:32792650,
	title = {Rheumatology - Immunology. University Lecture Notes for Internal Medicine and Rheumatology},
	url = {https://m2.mtmt.hu/api/publication/32792650},
	isbn = {9789633068588},
	author = {Kovács, László and Bocskai, Márta and Ladóczky-Hulló, Daniella and Kádár, Gabriella and Dobi, Diána and Balog, Attila and Burcsár, Szilárd},
	editor = {Kovács, László},
	publisher = {SZTE, Szent-Györgyi Albert Klinikai Központ, Reumatológiai és Immunológiai Klinika},
	unique-id = {32792650},
	year = {2022},
	orcid-numbers = {Kovács, László/0000-0003-4457-1430; Kovács, László/0000-0003-4457-1430}
}

@book{MTMT:32792611,
	title = {Reumatológia - Immunológia. Egyetemi jegyzet belgyógyászat és reumatológia tantárgyakhoz},
	url = {https://m2.mtmt.hu/api/publication/32792611},
	isbn = {9789633068557},
	author = {Kovács, László and Balog, Attila and Hemelein, Rita Adrienn and Kádár, Gabriella and Dobi, Diána and Burcsár, Szilárd and Bocskai, Márta and Ladóczky-Hulló, Daniella and Besenyi, Zsuzsanna},
	editor = {Kovács, László},
	publisher = {SZTE, Szent-Györgyi Albert Klinikai Központ, Reumatológiai és Immunológiai Klinika},
	unique-id = {32792611},
	year = {2022},
	orcid-numbers = {Kovács, László/0000-0003-4457-1430; Besenyi, Zsuzsanna/0000-0001-9115-9620; Kovács, László/0000-0003-4457-1430}
}

@article{MTMT:32076825,
	title = {Inorganic pyrophosphate is reduced in patients with systemic sclerosis},
	url = {https://m2.mtmt.hu/api/publication/32076825},
	author = {Hsu, Vivien M and Kozák, Eszter Zita and Li, Qiaoli and Bocskai, Márta and Schlesinger, Naomi and Rosenthal, Ann and McClure, Scott T and Kovács, László and Bálint, Bálint László and Szamosi, Szilvia and Szűcs, Gabriella and Carns, Mary and Aren, Kathleen and Goldberg, Isaac and Váradi, András and Varga, John},
	doi = {10.1093/rheumatology/keab508},
	journal-iso = {RHEUMATOLOGY},
	journal = {RHEUMATOLOGY (UNITED KINGDOM)},
	volume = {61},
	unique-id = {32076825},
	issn = {1462-0324},
	keywords = {CALCINOSIS; systemic sclerosis; Inorganic pyrophosphate},
	year = {2022},
	eissn = {1462-0332},
	pages = {1158-1165},
	orcid-numbers = {Kovács, László/0000-0003-4457-1430; Bálint, Bálint László/0000-0002-6163-7190}
}

@article{MTMT:32575652,
	title = {Integrative epigenomics in Sjögren´s syndrome reveals novel pathways and a strong interaction between the HLA, autoantibodies and the interferon signature},
	url = {https://m2.mtmt.hu/api/publication/32575652},
	author = {Teruel, M. and Barturen, G. and Martínez-Bueno, M. and Castellini-Pérez, O. and Barroso-Gil, M. and Povedano, E. and Kerick, M. and Català-Moll, F. and Makowska, Z. and Buttgereit, A. and Beretta, L. and Vigone, B. and Pers, J.-O. and Saraux, A. and Devauchelle-Pensec, V. and Cornec, D. and Jousse-Joulin, S. and Lauwerys, B. and Ducreux, J. and Maudoux, A.-L. and Vasconcelos, C. and Tavares, A. and Neves, E. and Faria, R. and Brandão, M. and Campar, A. and Marinho, A. and Farinha, F. and Almeida, I. and Mantecón, M.A.G.-G. and Alonso, R.B. and Martínez, A.C. and Cervera, R. and Rodríguez-Pintó, I. and Espinosa, G. and Lories, R. and De, Langhe E. and Hunzelmann, N. and Belz, D. and Witte, T. and Baerlecken, N. and Stummvoll, G. and Zauner, M. and Lehner, M. and Collantes, E. and Ortega-Castro, R. and Aguirre-Zamorano, M.ªA. and Escudero-Contreras, A. and Castro-Villegas, M.ªC. and Ortego, N. and Roldán, M.C.F. and Raya, E. and Moleón, I.J. and de, Ramon E. and Quintero, I.D. and Meroni, P.L. and Gerosa, M. and Schioppo, T. and Artusi, C. and Chizzolini, C. and Zuber, A. and Wynar, D. and Hiepe, F. and Gerl, V. and Thiel, S. and Maresca, M.R. and López-Berrio, A. and Aguilar-Quesada, R. and Navarro-Linares, H. and Alvarez, M. and Alvarez‑Errico, D. and Azevedo, N. and Barbarroja, N. and Buttgereit, A. and Cheng, Q. and Chizzolini, C. and Cremer, J. and De, Groof A. and De, Langhe E. and Ducreux, J. and Dufour, A. and Gerl, V. and Hernandez‑Fuentes, M. and Khodadadi, L. and Kniesch, K. and Li, T. and Lopez‑Pedrera, C. and Makowska, Z. and Marañón, C. and Muchmore, B. and Neves, E. and Rouvière, B. and Simon, Q. and Trombetta, E. and Varela, N. and Witte, T. and Pers, J.-O. and Marañón, C. and Ballestar, E. and Martin, J. and Carnero-Montoro, E. and Alarcón-Riquelme, M.E. and PRECISESADS, Clinical Consortium and PRECISESADS, Flow Cytometry Study Group},
	doi = {10.1038/s41598-021-01324-0},
	journal-iso = {SCI REP},
	journal = {SCIENTIFIC REPORTS},
	volume = {11},
	unique-id = {32575652},
	issn = {2045-2322},
	abstract = {Primary Sjögren’s syndrome (SS) is a systemic autoimmune disease characterized by lymphocytic infiltration and damage of exocrine salivary and lacrimal glands. The etiology of SS is complex with environmental triggers and genetic factors involved. By conducting an integrated multi-omics study, we confirmed a vast coordinated hypomethylation and overexpression effects in IFN-related genes, what is known as the IFN signature. Stratified and conditional analyses suggest a strong interaction between SS-associated HLA genetic variation and the presence of Anti-Ro/SSA autoantibodies in driving the IFN epigenetic signature and determining SS. We report a novel epigenetic signature characterized by increased DNA methylation levels in a large number of genes enriched in pathways such as collagen metabolism and extracellular matrix organization. We identified potential new genetic variants associated with SS that might mediate their risk by altering DNA methylation or gene expression patterns, as well as disease-interacting genetic variants that exhibit regulatory function only in the SS population. Our study sheds new light on the interaction between genetics, autoantibody profiles, DNA methylation and gene expression in SS, and contributes to elucidate the genetic architecture of gene regulation in an autoimmune population. © 2021, The Author(s).},
	year = {2021},
	eissn = {2045-2322},
	orcid-numbers = {Kovács, László/0000-0003-4457-1430}
}

@article{MTMT:32242154,
	title = {Az anorganikus pirofoszfát-szint vizsgálata sclerodermás betegeinkben},
	url = {https://m2.mtmt.hu/api/publication/32242154},
	author = {Bocskai, Márta and Kozák, E and Szamosi, Sz and Bálint, Bálint László and Horváth, Á and Szűcs, G and Váradi, A and Kovács, László},
	journal-iso = {MAGYAR REUMATOL},
	journal = {MAGYAR REUMATOLÓGIA},
	volume = {62},
	unique-id = {32242154},
	issn = {0139-4495},
	year = {2021},
	pages = {142},
	orcid-numbers = {Bálint, Bálint László/0000-0002-6163-7190; Kovács, László/0000-0003-4457-1430}
}