TY - JOUR AU - Szabó-Taylor, Katalin AU - Pálóczi, Krisztina AU - Szabó, Géza Tamás AU - Németh, Andrea AU - Osteikoetxea, Xabier AU - Sódar, Barbara AU - Holub Marianna, Csilla AU - Nyitrayné Pap, Erna AU - György, Bence AU - Pállinger, Éva AU - Szente-Pásztói, Mária AU - Buzás, Edit Irén TI - The role of post-translational modifications of microvesicles in systemic immune responses of mice JF - JOURNAL OF EXTRACELLULAR VESICLES J2 - J EXTRACELLULAR VESICL VL - 3 PY - 2014 IS - Suppl. 1 SP - 88 EP - 88 PG - 1 SN - 2001-3078 UR - https://m2.mtmt.hu/api/publication/2785400 ID - 2785400 LA - English DB - MTMT ER - TY - JOUR AU - Szabó, Géza Tamás AU - Tarr, B AU - Pálóczi, Krisztina AU - L. Éder, Katalin AU - Lajkó, Eszter AU - Kittel, Ágnes AU - Tóth, Sára AU - György, Bence AU - Szente-Pásztói, Mária AU - Németh, Andrea AU - Osteikoetxea, Xabier AU - Pállinger, Éva AU - Falus, András AU - Szabó-Taylor, Katalin AU - Buzás, Edit Irén TI - Critical role of extracellular vesicles in modulating the cellular effects of cytokines JF - CELLULAR AND MOLECULAR LIFE SCIENCES J2 - CELL MOL LIFE SCI VL - 71 PY - 2014 IS - 20 SP - 4055 EP - 4067 PG - 13 SN - 1420-682X DO - 10.1007/s00018-014-1618-z UR - https://m2.mtmt.hu/api/publication/2596795 ID - 2596795 N1 - K. Szabó-Taylor and E. I. Buzás contributed equally. AB - Under physiological and pathological conditions, extracellular vesicles (EVs) are present in the extracellular compartment simultaneously with soluble mediators. We hypothesized that cytokine effects may be modulated by EVs, the recently recognized conveyors of intercellular messages. In order to test this hypothesis, human monocyte cells were incubated with CCRF acute lymphoblastic leukemia cell line-derived EVs with or without the addition of recombinant human TNF, and global gene expression changes were analyzed. EVs alone regulated the expression of numerous genes related to inflammation and signaling. In combination, the effects of EVs and TNF were additive, antagonistic, or independent. The differential effects of EVs and TNF or their simultaneous presence were also validated by Taqman assays and ELISA, and by testing different populations of purified EVs. In the case of the paramount chemokine IL-8, we were able to demonstrate a synergistic upregulation by purified EVs and TNF. Our data suggest that neglecting the modulating role of EVs on the effects of soluble mediators may skew experimental results. On the other hand, considering the combined effects of cytokines and EVs may prove therapeutically useful by targeting both compartments at the same time. LA - English DB - MTMT ER - TY - JOUR AU - Bognár, Péter János AU - Nemeth, I AU - Mayer, Balázs AU - Haluszka, Dóra AU - Wikonkál, Norbert AU - Ostorházi, Eszter AU - John, S AU - Paulsson, M AU - Smyth, N AU - Szente-Pásztói, Mária AU - Buzás, Edit Irén AU - Szipőcs, Róbert AU - Kolonics, Attila AU - Temesvári, Erzsébet AU - Kárpáti, Sarolta TI - Reduced Inflammatory Threshold Indicates Skin Barrier Defect in Transglutaminase 3 Knockout Mice JF - JOURNAL OF INVESTIGATIVE DERMATOLOGY J2 - J INVEST DERMATOL VL - 134 PY - 2014 IS - 1 SP - 105 EP - 111 PG - 7 SN - 0022-202X DO - 10.1038/jid.2013.307 UR - https://m2.mtmt.hu/api/publication/2381023 ID - 2381023 AB - Recently a transglutaminase 3 knockout (TGM3/KO) mouse was generated that showed impaired hair development, but no gross defects in the epidermal barrier, although increased fragility of isolated corneocytes was demonstrated. Here we investigated the functionality of skin barrier in vivo by percutaneous sensitization to fluorescein-isothiocyanate (FITC) in TGM3/KO (n=64) and C57BL/6 WT mice (n=36). Cutaneous inflammation was evaluated by mouse ear swelling test (MEST), histology, serum IgE levels, and by flow-cytometry from draining lymph nodes. Inflammation induced significant MEST difference (P<0.0001) was detected between KO and WT mice and was supported also by histopathology. A significant increase of CD4+ CD25+ activated T-cells (P<0.01) and elevated serum IgE levels (P<0.05) in KO mice indicated more the development of FITC sensibilization than an irritative reaction. P. acnes induced intracutaneous inflammation showed no difference (P=0.2254) between the reactivity of WT and KO immune system. As in vivo tracer, FITC penetration from skin surface followed by two-photon microscopy demonstrated a more invasive percutaneous penetration in KO mice. The clinically uninvolved skin in TGM3/KO mice showed impaired barrier function and higher susceptibility to FITC sensitization indicating that TGM3 has a significant contribution to the functionally intact cutaneous barrier.Journal of Investigative Dermatology accepted article preview online, 24 July 2013. doi:10.1038/jid.2013.307. LA - English DB - MTMT ER - TY - JOUR AU - Misják, Petra AU - Bősze, Szilvia AU - Horváti, Kata AU - Szente-Pásztói, Mária AU - Pálóczi, Krisztina AU - Holub Marianna, Csilla AU - Szakacs, F AU - Aradi, B AU - György, Bence AU - Szabó, Géza Tamás AU - Nagy, György AU - Glant, TT AU - Mikecz, K AU - Falus, András AU - Buzás, Edit Irén TI - The role of citrullination of an immunodominant proteoglycan (PG) aggrecan T cell epitope in BALB/c mice with PG-induced arthritis JF - IMMUNOLOGY LETTERS J2 - IMMUNOL LETT VL - 152 PY - 2013 IS - 1 SP - 25 EP - 31 PG - 7 SN - 0165-2478 DO - 10.1016/j.imlet.2013.03.005 UR - https://m2.mtmt.hu/api/publication/2320082 ID - 2320082 N1 - Department of Genetics Cell- and Immunobiology, Semmelweis University, Budapest, Hungary Department of Organic Chemistry, L. Eötvös University, Budapest, Hungary Research Group for Inflammation Biology and Immunogenomics, Hungarian Academy of Sciences, Budapest, Hungary Department of Rheumatology, Semmelweis University, Budapest, Hungary Section of Molecular Medicine, Department of Orthopedic Surgery, Rush University Medical Center, Chicago, IL, United States Cited By :10 Export Date: 22 May 2023 CODEN: IMLED Correspondence Address: Buzás, E.I.; Semmelweis University, Nagyváradtér 4, Budapest H-1089, Hungary; email: edit.buzas@gmail.com AB - The P70-84 peptide (also called 5/4E8 epitope) of the human cartilage proteoglycan (PG) aggrecan is the dominant/arthritogenic epitope in both humans and arthritis-prone BALB/c mice (PG-induced arthritis, PGIA). An elevated T cell reactivity was demonstrated to a citrullinated version of the P70-84 epitope in most of the patients with rheumatoid arthritis (RA). The goal of this study was to understand better how a T cell epitope, if citrullinated, may affect antigenicity/arthritogenicity in PGIA, a murine model of RA. T cell reactivity to differentially citrullinated versions of either the human PG aggrecan P70-84 peptide or the corresponding mouse sequence was assessed in peptide or aggrecan-immunized and arthritic BALB/c mice as well as in T cell receptor transgenic mice specific for peptide P70-84 sequence. Peripheral T cell responses were induced by priming BALB/c mice with either the human wild-type or its citrullinated versions. Unexpectedly, priming with the citrullinated self-peptide induced a higher T cell response compared to the wild-type sequence (p<0.001), and the citrullination of the human peptide abolished T cell reactivity in PGIA. Our data suggest that T cells reactive to the citrullinated P70-84 peptide escaped thymic selection and are present in the peripheral T cell repertoire. Results of this study provide evidence that citrullination of an immunodominant T cell epitope may substantially alter, either increase or abolish, T cell recognition at the periphery in an experimental model of arthritis. LA - English DB - MTMT ER - TY - JOUR AU - Szente-Pásztói, Mária AU - Sódar, Barbara AU - Misják, Petra AU - Pálóczi, Krisztina AU - Kittel, Ágnes AU - Tóth, Kálmán AU - Wellinger, Károly AU - Géher, Pál AU - Nagy, György AU - Lakatos, T AU - Falus, András AU - Buzás, Edit Irén TI - The recently identified hexosaminidase D enzyme substantially contributes to the elevated hexosaminidase activity in rheumatoid arthritis JF - IMMUNOLOGY LETTERS J2 - IMMUNOL LETT VL - 149 PY - 2013 IS - 1-2 SP - 71 EP - 76 PG - 6 SN - 0165-2478 DO - 10.1016/j.imlet.2012.10.012 UR - https://m2.mtmt.hu/api/publication/2105621 ID - 2105621 N1 - Department of Genetics, Cell and Immunobiology, Semmelweis University, Nagyvárad tér 4, Budapest, H-1089, Hungary Inflammation Biology and Immunogenomics Research Group, Hungarian Academy of Sciences-Semmelweis University, Nagyvárad tér 4, Budapest, H-1089, Hungary Institute of Experimental Medicine, Hungarian Academy of Sciences, Szigony u. 43, Budapest, H-1083, Hungary Department of Orthopedic Surgery, Szeged University, Semmelweis u.6, Szeged, H-6725, Hungary Department of Rheumatology, Semmelweis University, Frankel Leó utca 54, Budapest, H-1027, Hungary Cited By :18 Export Date: 5 August 2019 CODEN: IMLED Correspondence Address: Buzás, E.I.; Department of Genetics, Cell and Immunobiology, Semmelweis University, Nagyvárad tér 4, Budapest, H-1089, Hungary; email: edit.buzas@gmail.com Department of Genetics, Cell and Immunobiology, Semmelweis University, Nagyvárad tér 4, Budapest, H-1089, Hungary Inflammation Biology and Immunogenomics Research Group, Hungarian Academy of Sciences-Semmelweis University, Nagyvárad tér 4, Budapest, H-1089, Hungary Institute of Experimental Medicine, Hungarian Academy of Sciences, Szigony u. 43, Budapest, H-1083, Hungary Department of Orthopedic Surgery, Szeged University, Semmelweis u.6, Szeged, H-6725, Hungary Department of Rheumatology, Semmelweis University, Frankel Leó utca 54, Budapest, H-1027, Hungary Cited By :18 Export Date: 7 August 2019 CODEN: IMLED Correspondence Address: Buzás, E.I.; Department of Genetics, Cell and Immunobiology, Semmelweis University, Nagyvárad tér 4, Budapest, H-1089, Hungary; email: edit.buzas@gmail.com Funding Agency and Grant Number: [OTKA 73247]; [OTKA 84043]; [FP7-PEOPLE-2011-ITN - PITN-GA-2011-289033 "DYNANO"] Funding text: This work was supported by research grants OTKA 73247, OTKA 84043 and FP7-PEOPLE-2011-ITN - PITN-GA-2011-289033 "DYNANO". Department of Genetics, Cell and Immunobiology, Semmelweis University, Nagyvárad tér 4, Budapest, H-1089, Hungary Inflammation Biology and Immunogenomics Research Group, Hungarian Academy of Sciences-Semmelweis University, Nagyvárad tér 4, Budapest, H-1089, Hungary Institute of Experimental Medicine, Hungarian Academy of Sciences, Szigony u. 43, Budapest, H-1083, Hungary Department of Orthopedic Surgery, Szeged University, Semmelweis u.6, Szeged, H-6725, Hungary Department of Rheumatology, Semmelweis University, Frankel Leó utca 54, Budapest, H-1027, Hungary Cited By :19 Export Date: 18 April 2020 CODEN: IMLED Correspondence Address: Buzás, E.I.; Department of Genetics, Cell and Immunobiology, Semmelweis University, Nagyvárad tér 4, Budapest, H-1089, Hungary; email: edit.buzas@gmail.com Chemicals/CAS: beta n acetylhexosaminidase, 37211-57-7, 9012-33-3, 9027-52-5; beta-N-Acetylhexosaminidases, 3.2.1.52 LA - English DB - MTMT ER - TY - JOUR AU - Szabó, Géza Tamás AU - Misják, Petra AU - Aradi, B AU - György, Bence AU - Szente-Pásztói, Mária AU - Pál, Zsuzsanna AU - László, Valéria AU - Pállinger, Éva AU - Nyitrayné Pap, Erna AU - Kittel, A AU - Nagy, György AU - Falus, András AU - Buzás, Edit Irén TI - Meta-analysis of exosomal and microvesicular proteoms from the aspect of autoimmunity JF - EUROPEAN JOURNAL OF CLINICAL INVESTIGATION J2 - EUR J CLIN INVEST VL - 42 PY - 2012 IS - 1 SP - 68 EP - 68 PG - 1 SN - 0014-2972 UR - https://m2.mtmt.hu/api/publication/2089636 ID - 2089636 LA - English DB - MTMT ER - TY - JOUR AU - György, Bence AU - Szente-Pásztói, Mária AU - Buzás, Edit Irén TI - Systematic use of Triton lysis as a control for microvesicle labeling JF - BLOOD J2 - BLOOD VL - 119 PY - 2012 IS - 9 SP - 2175 EP - 2176 PG - 2 SN - 0006-4971 DO - 10.1182/blood-2012-01-401091 UR - https://m2.mtmt.hu/api/publication/2089619 ID - 2089619 LA - English DB - MTMT ER - TY - JOUR AU - György, Bence AU - Módos, Károly AU - Pállinger, Éva AU - Pálóczi, Krisztina AU - Szente-Pásztói, Mária AU - Misják, Petra AU - Deli, MA AU - Sipos, A AU - Szalai, A AU - Voszka, István AU - Polgár, A AU - Tóth, K AU - Csete, M AU - Nagy, György AU - Gay, S AU - Falus, András AU - Kittel, A AU - Buzás, Edit Irén TI - Diagnostic assessment of cell-derived microparticles in rheumatoid arthritis is falsified by immune complexes. JF - ANNALS OF THE RHEUMATIC DISEASES J2 - ANN RHEUM DIS VL - 70 PY - 2011 IS - Suppl 3 SP - 717 SN - 0003-4967 UR - https://m2.mtmt.hu/api/publication/2118722 ID - 2118722 N1 - EULAR 2011 London, United Kingdom LA - English DB - MTMT ER - TY - JOUR AU - Szente-Pásztói, Mária AU - Falus, András AU - Buzás, Edit Irén TI - Ízületek autoimmun megbetegedéseinek „édes” (szénhidrát-biológiai) vonatkozásai JF - MAGYAR TUDOMÁNY J2 - MAGYAR TUDOMÁNY VL - 172 PY - 2011 IS - 11 SP - 1346 EP - 1354 PG - 9 SN - 0025-0325 UR - https://m2.mtmt.hu/api/publication/2118082 ID - 2118082 LA - Hungarian DB - MTMT ER - TY - JOUR AU - Szente-Pásztói, Mária AU - Misják, Petra AU - György, Bence AU - Aradi, B AU - Szabó, Géza Tamás AU - Szántó, B AU - Holub Marianna, Csilla AU - Nagy, György AU - Falus, András AU - Buzás, Edit Irén TI - Infection and autoimmunity. Lessons of animal models TS - Lessons of animal models JF - EUROPEAN JOURNAL OF MICROBIOLOGY AND IMMUNOLOGY J2 - EUR J MICROBIOL IMMU VL - 1 PY - 2011 IS - 3 SP - 198 EP - 207 PG - 10 SN - 2062-509X DO - 10.1556/EuJMI.1.2011.3.3 UR - https://m2.mtmt.hu/api/publication/2118080 ID - 2118080 N1 - Funding Agency and Grant Number: OTKA [K73247, 84043, 77537, 83857] Funding text: This work was supported by grants OTKA K73247, 84043, 77537 and 83857. LA - English DB - MTMT ER -