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1.

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)
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2.

001-es BibID:BIBFORM073625
Első szerző:Egelston, Colt
Cím:Suppression of dendritic cell maturation and T cell proliferation by synovial fluid myeloid cells from mice with autoimmune arthritis / Colt Egelston, Júlia Kurkó, Timea Besenyei, Beata Tryniszewska, Tibor A. Rauch, Tibor T. Glant, Katalin Mikecz
Dátum:2012
ISSN:0004-3591 1529-0131
Megjegyzések:OBJECTIVE:To determine whether myeloid cells (such as granulocytes) present in the synovial fluid (SF) of arthritic joints have an impact on adaptive immunity. Specifically, we investigated the effects of SF cells harvested from the joints of mice with proteoglycan-induced arthritis (PGIA), on dendritic cell (DC) maturation and antigen-specific T cell proliferation.METHODS:We monitored DC maturation (MHCII and CD86 expression) by flow cytometry upon coculture of DCs with SF cells or spleen myeloid cells from mice with PGIA. The effects of these myeloid cells on T cell proliferation were studied using T cells purified from PG-specific T cell receptor (TCR)-transgenic (Tg) mice. Phenotype analysis of myeloid cells was performed by immunostaining, reverse transcription-polymerase chain reaction, Western blotting, and biochemical assays.RESULTS:Inflammatory SF cells significantly suppressed the maturation of DCs upon coculture. PG-TCR-Tg mouse T cells cultured with antigen-loaded DCs showed dramatic decreases in proliferation in the presence of SF cells. Spleen myeloid cells from arthritic mice did not have suppressive effects. SF cells were unable to suppress CD3/CD28-stimulated proliferation of the same T cells, suggesting a DC-dependent mechanism. SF cells exhibited all of the characteristics of myeloid-derived suppressor cells (MDSCs) and exerted suppression primarily through the production of nitric oxide and reactive oxygen species by granulocyte-like cells.CONCLUSION:SF in the joints of mice with PGIA contains a population of granulocytic MDSCs that potently suppress DC maturation and T cell proliferation. These MDSCs have the potential to limit the expansion of autoreactive T cells, thus breaking the vicious cycle of autoimmunity and inflammation.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Arthritis and Rheumatism 64 : 10 (2012), p. 3179-3188. -
További szerzők:Kurkó Júlia Emese (1979-) (reumatológus) Besenyei Tímea (1980-) (reumatológus, belgyógyász) Tryniszewska Beáta Rauch Tibor A. Glant Tibor T. Mikecz Katalin
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3.

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.
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4.

001-es BibID:BIBFORM093466
Első szerző:Kurkó Júlia Emese (reumatológus)
Cím:Myeloid-Derived Suppressor Cells Present in the Synovial Fluid of Mice with Proteoglycan-Induced Arthritis Are Potent Suppressors of Dendritic Cell Maturation and T Cell Proliferation / Julia Kurko, Colt Egelston, Timea Besenyei, Beata Tryniszewska, Tamas Kobezda, Tibor A. Rauch, Tibor T. Glant, Katalin Mikecz
Dátum:2011
Tárgyszavak:Orvostudományok Klinikai orvostudományok idézhető absztrakt
folyóiratcikk
Megjelenés:Arthritis & Rheumatism. - 63 : Suppl10 (2011), p. S393. -
További szerzők:Egelston, Colt Besenyei Tímea (1980-) (reumatológus, belgyógyász) Tryniszewska Beáta Kobezda Tamás (1983-) (Ph.D hallgató) Rauch Tibor A. Glant Tibor T. Mikecz Katalin
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5.

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
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