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Your search keyword '"Olasz, Katalin"' showing total 22 results
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22 results on '"Olasz, Katalin"'

2. The immunological role of the spleen in autoimmune arthritis: lessons from mice with genetic spleen disorganisation or splenectomy.

Author

KHANFAR, ESAM, OLASZ, KATALIN, GÁL, SZONJA, BALOGH, PÉTER, BERKI, TÍMEA, and BOLDIZSÁR, FERENC

Subjects
SPLEEN, INNATE lymphoid cells, B cells, ARTHRITIS, SPLENECTOMY, IMMUNE serums, AUTOIMMUNITY
Abstract

Copyright of Immunology Quaterly / Immunologiai Szemle is the property of Medicina Konyvkiado Zrt. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Published
2024

21. Spontaneous Insertion of a B2 Element in the Ptpn6Gene Drives a Systemic Autoinflammatory Disease in Mice Resembling Neutrophilic Dermatosis in Humans

Author

Nesterovitch, Andrew B., Szanto, Sandor, Gonda, Andrea, Bardos, Tamas, Kis-Toth, Katalin, Adarichev, Vyacheslav A., Olasz, Katalin, Ghassemi-Najad, Sheida, Hoffman, Mark D., Tharp, Michael D., Mikecz, Katalin, and Glant, Tibor T.

Abstract

We found a spontaneous autosomal mutation in a mouse leading to neutrophil infiltration with ulceration in the upper dermis of homozygous offspring. These animals had increased neutrophil numbers, associated with normal lymphocyte count, in peripheral blood and bone marrow, suggesting a myeloproliferative disorder; however, granulocyte precursor proliferation in bone marrow was actually reduced (because circulating neutrophils were less susceptible to apoptosis). Neutrophil infiltration of the skin and other organs and high serum levels of immunoglobulins and autoantibodies, cytokines, and acute-phase proteins were additional abnormalities, all of which could be reduced by high-dose corticosteroid treatment or neutrophil depletion by antibodies. Use of genome-wide screening localized the mutation within an 0.4-Mbp region on mouse chromosome 6. We identified insertion of a B2 element in exon 6 of the Ptpn6gene (protein tyrosine phosphatase, non-receptor type 6; also known as Shp-1). This insertion involves amino acid substitutions that significantly reduced the enzyme activity in mice homozygous for the mutation. Disease onset was delayed, and the clinical phenotype was milder than the phenotypes of other Ptpn6-mutants described in motheaten (me, mev) mice; we designated this new genotype as Ptpn6meB2/meB2and the phenotype as meB2. This new phenotype encompasses an autoinflammatory disease showing similarities to many aspects of the so-called neutrophilic dermatoses, a heterogeneous group of skin diseases with unknown etiology in humans.

Published
2011
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22. Ameliorated Autoimmune Arthritis and Impaired B Cell Receptor-Mediated Ca 2+ Influx in Nkx2-3 Knock-out Mice.

Author

Khanfar E, Olasz K, Gábris F, Gajdócsi E, Botz B, Kiss T, Kugyelka R, Berki T, Balogh P, and Boldizsár F

Subjects
Aggrecans adverse effects, Aggrecans immunology, Animals, Arthritis, Experimental chemically induced, Arthritis, Experimental metabolism, Arthritis, Rheumatoid chemically induced, Arthritis, Rheumatoid metabolism, Calcium Signaling, Cells, Cultured, Cytokines metabolism, Female, Humans, Mice, Mice, Inbred BALB C, Mice, Knockout, Protein Domains, Severity of Illness Index, Spleen cytology, Spleen metabolism, Aggrecans chemistry, Arthritis, Experimental genetics, Arthritis, Rheumatoid genetics, B-Lymphocytes metabolism, Homeodomain Proteins genetics, Transcription Factors genetics
Abstract

B cells play a crucial role in the pathogenesis of rheumatoid arthritis. In Nkx2-3-deficient mice (Nkx2-3 -/- ) the spleen's histological structure is fundamentally changed; therefore, B cell homeostasis is seriously disturbed. Based on this, we were curious, whether autoimmune arthritis could be induced in Nkx2-3 -/- mice and how B cell activation and function were affected. We induced arthritis with immunization of recombinant human proteoglycan aggrecan G1 domain in Nkx2-3 -/- and control BALB/c mice. We followed the clinical picture, characterized the radiological changes, the immune response, and intracellular Ca 2+ signaling of B cells. Incidence of the autoimmune arthritis was lower, and the disease severity was milder in Nkx2-3 -/- mice than in control BALB/c mice. The radiological changes were in line with the clinical picture. In Nkx2-3 -/- mice, we measured decreased antigen-induced proliferation and cytokine production in spleen cell cultures; in the sera, we found less anti-CCP-IgG2a, IL-17 and IFNγ, but more IL-1β, IL-4 and IL-6. B cells isolated from the lymph nodes of Nkx2-3 -/- mice showed decreased intracellular Ca 2+ signaling compared to those isolated from BALB/c mice. Our findings show that the transcription factor Nkx2-3 might regulate the development of autoimmune arthritis most likely through modifying B cell activation.

Published
2020
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