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Your search keyword '"Kania, Gabriela"' showing total 9 results
Start Over Author "Kania, Gabriela" Publisher elsevier bv
9 results on '"Kania, Gabriela"'

1. The AP1 Transcription Factor Fosl2 Promotes Systemic Autoimmunity and Inflammation by Repressing Treg Development

Author

Renoux, Florian, primary, Stellato, Mara, additional, Haftmann, Claudia, additional, Vogetseder, Alexander, additional, Huang, Riyun, additional, Subramaniam, Arun, additional, Becker, Mike O., additional, Blyszczuk, Przemyslaw, additional, Becher, Burkhard, additional, Distler, Jörg H.W., additional, Kania, Gabriela, additional, Boyman, Onur, additional, and Distler, Oliver, additional

Published
2020
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2. Uptake and bioreactivity of charged chitosan-coated superparamagnetic nanoparticles as promising contrast agents for magnetic resonance imaging

Author

Kania, Gabriela, primary, Sternak, Magdalena, additional, Jasztal, Agnieszka, additional, Chlopicki, Stefan, additional, Błażejczyk, Agnieszka, additional, Nasulewicz-Goldeman, Anna, additional, Wietrzyk, Joanna, additional, Jasiński, Krzysztof, additional, Skórka, Tomasz, additional, Zapotoczny, Szczepan, additional, and Nowakowska, Maria, additional

Published
2018
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4. Abnormal High-Density Lipoprotein Induces Endothelial Dysfunction via Activation of Toll-like Receptor-2

Author

Speer, Thimoteus, primary, Rohrer, Lucia, additional, Blyszczuk, Przemyslaw, additional, Shroff, Rukshana, additional, Kuschnerus, Kira, additional, Kränkel, Nicolle, additional, Kania, Gabriela, additional, Zewinger, Stephen, additional, Akhmedov, Alexander, additional, Shi, Yi, additional, Martin, Tina, additional, Perisa, Damir, additional, Winnik, Stephan, additional, Müller, Maja F., additional, Sester, Urban, additional, Wernicke, Gabriel, additional, Jung, Andreas, additional, Gutteck, Ursula, additional, Eriksson, Urs, additional, Geisel, Jürgen, additional, Deanfield, John, additional, von Eckardstein, Arnold, additional, Lüscher, Thomas F., additional, Fliser, Danilo, additional, Bahlmann, Ferdinand H., additional, and Landmesser, Ulf, additional

Published
2013
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9. GM-CSF promotes inflammatory dendritic cell formation but does not contribute to disease progression in experimental autoimmune myocarditis

Author

Gabriela Kania, Thomas F. Lüscher, Urs Eriksson, Silvia Behnke, Przemyslaw Blyszczuk, University of Zurich, and Kania, Gabriela

Subjects
Adoptive cell transfer, T-Lymphocytes, Gene Expression, 030204 cardiovascular system & hematology, Monocytes, 1307 Cell Biology, Mice, 0302 clinical medicine, Cell Movement, Mice, Inbred BALB C, Inflammatory dendritic cells, 0303 health sciences, biology, Adoptive Transfer, 3. Good health, Myocarditis, medicine.anatomical_structure, Integrin alpha M, 10076 Center for Integrative Human Physiology, Disease Progression, 10209 Clinic for Cardiology, medicine.symptom, Signal Transduction, T cell, CD11c, 610 Medicine & health, Inflammation, Myosins, Autoimmune Diseases, 03 medical and health sciences, Antigens, CD, 1312 Molecular Biology, medicine, Animals, Inflammatory progenitors, Molecular Biology, Cell Proliferation, 030304 developmental biology, Myocardium, Granulocyte-Macrophage Colony-Stimulating Factor, GM-CSF, Dendritic Cells, Dendritic cell, Cell Biology, medicine.disease, Disease Models, Animal, Immunology, biology.protein, 570 Life sciences, Immunization, Biomarkers, CD80
Abstract

Background Granulocyte macrophage-colony stimulating factor (GM-CSF) is critically required for the induction of experimental autoimmune myocarditis (EAM), a model of post-inflammatory dilated cardiomyopathy. Its specific role in the progression of myocarditis into end stage heart failure is not known. Methods and results BALB/c mice were immunized with myosin peptide and complete Freund's adjuvant at days 0 and 7. Heart-infiltrating inflammatory CD133+ progenitors were isolated from inflamed hearts at the peak of inflammation (day 21). In the presence of GM-CSF, inflammatory CD133+ progenitors up-regulated integrin, alpha X (CD11c), class II major histocompatibility complex, CD80 and CD86 co-stimulatory molecules reflecting an inflammatory dendritic cell (DC) phenotype. Inflammatory DCs stimulated antigen-specific CD4+ T cell proliferation and induced myocarditis after myosin peptide loading and adoptive transfer in healthy mice. Moreover, GM-CSF treatment of mice after the peak of disease, between days 21 and 29 of EAM, transiently increased accumulation of inflammatory DCs in the myocardium. Importantly, bone marrow-derived CD11b+ monocytes, rather than inflammatory CD133+ progenitors represent the dominant cellular source of heart-infiltrating inflammatory DCs in EAM. In contrast, GM-CSF treatment neither affected numbers of heart-infiltrating CD45+ and CD3+ T cells nor the development of post-inflammatory fibrosis. Conclusions GM-CSF treatment promotes formation of inflammatory DCs in EAM. In contrast to the active roles of GM-CSF and DCs in EAM induction, GM-CSF-induced inflammatory DCs neither prevent resolution of active inflammation, nor contribute to post-inflammatory cardiac remodelling. This article is part of a Special Issue entitled: Cardiomyocyte Biology: Cardiac Pathways of Differentiation, Metabolism and Contraction.

Published
2013
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