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001-es BibID:	BIBFORM044036
Első szerző:	Besenyei Tímea (reumatológus, belgyógyász)
Cím:	Non-MHC Risk Alleles in Rheumatoid Arthritis and in the Syntenic Chromosome Regions of Corresponding Animal Models / Besenyei Timea, Kadar Andras, Tryniszewska Beata, Kurko Julia, Rauch Tibor A., Glant Tibor T., Mikecz Katalin, Szekanecz Zoltan
Dátum:	2012
ISSN:	1740-2522
Megjegyzések:	Rheumatoid arthritis (RA) is a polygenic autoimmune disease primarily affecting the synovial joints. Numerous animal models show similarities to RA in humans; some of them not only mimic the clinical phenotypes but also demonstrate the involvement of homologous genomic regions in RA. This paper compares corresponding non-MHC genomic regions identified in rodent and human genome-wide association studies (GWAS). To date, over 30 non-MHC RA-associated loci have been identified in humans, and over 100 arthritis-associated loci have been identified in rodent models of RA. The genomic regions associated with the disease are designated by the name(s) of the gene having the most frequent and consistent RA-associated SNPs or a function suggesting their involvement in inflammatory or autoimmune processes. Animal studies on rats and mice preferentially have used single sequence length polymorphism (SSLP) markers to identify disease-associated qualitative and quantitative trait loci (QTLs) in the genome of F2 hybrids of arthritis-susceptible and arthritis-resistant rodent strains. Mouse GWAS appear to be far ahead of rat studies, and significantly more mouse QTLs correspond to human RA risk alleles
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Rheumatoid arthritis polygenic autoimmune disease
Megjelenés:	Clinical And Development Immunology. - 2012 (2012), p. 1-14. -
További szerzők:	Kádár András (1977-) (belgyógyász) Tryniszewska Beáta Kurkó Júlia Emese (1979-) (reumatológus) Rauch Tibor A. Glant Tibor T. Mikecz Katalin Szekanecz Zoltán (1964-) (reumatológus, belgyógyász, immunológus)
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM050381
035-os BibID:	PMID:23653330
Első szerző:	Glant Tibor T.
Cím:	Differentially expressed epigenome modifiers, including aurora kinases A and B, in immune cells in rheumatoid arthritis in humans and mouse models / Tibor T. Glant, Timea Besenyei, András Kádár, Júlia Kurkó, Beata Tryniszewska, János Gál, Györgyi Soós, Zoltán Szekanecz, Gyula Hoffmann, Joel A. Block, Robert S. Katz, Katalin Mikecz, Tibor A. Rauch
Dátum:	2013
ISSN:	0004-3591
Megjegyzések:	To identify epigenetic factors that are implicated in the pathogenesis of rheumatoid arthritis (RA), and to explore the therapeutic potential of the targeted inhibition of these factors. METHODS: Polymerase chain reaction (PCR) arrays were used to investigate the expression profile of genes that encode key epigenetic regulator enzymes. Mononuclear cells from RA patients and mice were monitored for gene expression changes, in association with arthritis development in murine models of RA. Selected genes were further characterized by quantitative reverse transcription-PCR, Western blot, and flow cytometry methods. The targeted inhibition of the up-regulated enzymes was studied in arthritic mice. RESULTS: A set of genes with arthritis-specific expression was identified by the PCR arrays. Aurora kinases A and B, both of which were highly expressed in arthritic mice and treatment-naive RA patients, were selected for detailed analysis. Elevated aurora kinase expression was accompanied by increased phosphorylation of histone H3, which promotes proliferation of T lymphocytes. Treatment with VX-680, a pan-aurora kinase inhibitor, promoted B cell apoptosis, provided significant protection against disease onset, and attenuated inflammatory reactions in arthritic mice. CONCLUSION: Arthritis development is accompanied by changes in expression of a number of epigenome-modifying enzymes. Drug-induced down-regulation of the aurora kinases, among other targets, seems to be sufficient to treat experimental arthritis. Development of new therapeutics that target aurora kinases can potentially improve RA management.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban epigenome modifiers rheumatoid arthritis
Megjelenés:	Arthritis and Rheumatism. - 65 : 7 (2013), p. 1725-1735. -
További szerzők:	Besenyei Tímea (1980-) (reumatológus, belgyógyász) Kádár András (1977-) (belgyógyász) Kurkó Júlia Emese (1979-) (reumatológus) Tryniszewska Beáta Gál János Soós Györgyike (1959-) (pathológus) Szekanecz Zoltán (1964-) (reumatológus, belgyógyász, immunológus) Hoffmann Gyula Block, Joel A. Katz, Robert S. Mikecz Katalin Rauch Tibor A.
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM056679
Első szerző:	Kurkó Júlia Emese (reumatológus)
Cím:	Suppression of proteoglycan-induced autoimmune arthritis by myeloid-derived suppressor cells generated In Vitro from Murine Bone Marrow / Júlia Kurkó, András Vida, Tímea Ocskó , Beata Tryniszewska, Tibor A. Rauch, Tibor T. Glant, Zoltán Szekanecz, Katalin Mikecz
Dátum:	2014
ISSN:	1932-6203
Megjegyzések:	Background: Myeloid-derived suppressor cells (MDSCs) are innate immune cells capable of suppressing T-cell responses. We previously reported the presence of MDSCs with a granulocytic phenotype in the synovial fluid (SF) of mice with proteoglycan (PG)-induced arthritis (PGIA), a T cell-dependent autoimmune model of rheumatoid arthritis (RA). However, the limited amount of SF-MDSCs precluded investigations into their therapeutic potential. The goals of this study were to develop an in vitro method for generating MDSCs similar to those found in SF and to reveal the therapeutic effect of such cells in PGIA. Methods: Murine bone marrow (BM) cells were cultured for 3 days in the presence of granulocyte macrophage colonystimulating factor (GM-CSF), interleukin-6 (IL-6), and granulocyte colony-stimulating factor (G-CSF). The phenotype of cultured cells was analyzed using flow cytometry, microscopy, and biochemical methods. The suppressor activity of BMMDSCs was tested upon co-culture with activated T cells. To investigate the therapeutic potential of BM-MDSCs, the cells were injected into SCID mice at the early stage of adoptively transferred PGIA, and their effects on the clinical course of arthritis and PG-specific immune responses were determined. Results: BM cells cultured in the presence of GM-CSF, IL-6, and G-CSF became enriched in MDSC-like cells that showed greater phenotypic heterogeneity than MDSCs present in SF. BM-MDSCs profoundly inhibited both antigen-specific and polyclonal T-cell proliferation primarily via production of nitric oxide. Injection of BM-MDSCs into mice with PGIA ameliorated arthritis and reduced PG-specific T-cell responses and serum antibody levels. Conclusions: Our in vitro enrichment strategy provides a SF-like, but controlled microenvironment for converting BM myeloid precursors into MDSCs that potently suppress both T-cell responses and the progression of arthritis in a mouse model of RA. Our results also suggest that enrichment of BM in MDSCs could improve the therapeutic efficacy of BM transplantation in RA.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Plos One. - 9 : 11 (2014), p. 1-14. -
További szerzők:	Vida András (1979-) (molekuláris biológus, genetikus) Ocskó Tímea Tryniszewska Beáta Rauch Tibor A. Glant Tibor T. Szekanecz Zoltán (1964-) (reumatológus, belgyógyász, immunológus) Mikecz Katalin
Pályázati támogatás:	TÁMOP4.2.4.A/2-11-1-2012-0001 TÁMOP
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM093463
Első szerző:	Vida András (molekuláris biológus, genetikus)
Cím:	Arthritis Associated Sequence Alterations Within a Genetic Susceptibility Region Of Mouse Chromosome 3; A Genomic Region Which Is Syntenic With a Prominent Non-MHC Locus In Rheumatoid Arthritis / Andras Vida, Timea Besenyei, Beata Tryniszewska, Timea Ocsko, Zoltan Szekanecz, Tibor A. Rauch, Katalin Mikecz, Tibor T. Glant
Dátum:	2013
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idézhető absztrakt folyóiratcikk
Megjelenés:	Arthritis & Rheumatism. - 65 : Suppl10 (2013), p. S808. -
További szerzők:	Besenyei Tímea (1980-) (reumatológus, belgyógyász) Tryniszewska Beáta Ocskó Tímea Szekanecz Zoltán (1964-) (reumatológus, belgyógyász, immunológus) Rauch Tibor A. Mikecz Katalin Glant Tibor T.
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat
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