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20 results on '"Marczynska, Joanna"'

5. The protective effect of Angiotensin AT2-receptor stimulation in Neuromyelitis optica spectrum disorder is independent of astrocyte-derived BDNF

Author

Khorooshi, Reza, primary, Marczynska, Joanna, additional, Dubik, Magdalena, additional, Dieu, Ruthe Storgaard, additional, Sørensen, Sofie Forsberg, additional, Montanana-Rosell, Roser, additional, Limburg, Hannah Liska, additional, Tygesen, Camilla, additional, Asgari, Nasrin, additional, Steckelings, Ulrike Muscha, additional, and Owens, Trevor, additional

Published
2021
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6. Central Nervous System-Endogenous TLR7 and TLR9 Induce Different Immune Responses and Effects on Experimental Autoimmune Encephalomyelitis

Author

Dieu, Ruthe Storgaard, primary, Wais, Vian, additional, Sørensen, Michael Zaucha, additional, Marczynska, Joanna, additional, Dubik, Magdalena, additional, Kavan, Stephanie, additional, Thomassen, Mads, additional, Burton, Mark, additional, Kruse, Torben, additional, Khorooshi, Reza, additional, and Owens, Trevor, additional

Published
2021
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10. Type I interferon‐activated microglia are critical for neuromyelitis optica pathology

Author

Wlodarczyk, Agnieszka, primary, Khorooshi, Reza, additional, Marczynska, Joanna, additional, Holtman, Inge R., additional, Burton, Mark, additional, Jensen, Kirstine Nolling, additional, Blaabjerg, Morten, additional, Meyer, Morten, additional, Thomassen, Mads, additional, Eggen, Bart J. L., additional, Asgari, Nasrin, additional, and Owens, Trevor, additional

Published
2020
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11. Protective roles for myeloid cells in neuroinflammation

Author

Owens, Trevor, primary, Benmamar‐Badel, Anouk, additional, Wlodarczyk, Agnieszka, additional, Marczynska, Joanna, additional, Mørch, Marlene T., additional, Dubik, Magdalena, additional, Arengoth, Dina S., additional, Asgari, Nasrin, additional, Webster, Gill, additional, and Khorooshi, Reza, additional

Published
2020
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12. MSJ860327_supplementary_material – Supplemental material for Angiotensin AT2 receptor–induced interleukin-10 attenuates neuromyelitis optica spectrum disorder–like pathology

Author

Khorooshi, Reza, Tofte-Hansen, Emil Ulrikkaholm, Tygesen, Camilla, Montanana-Rosell, Roser, Limburg, Hannah Liska, Marczynska, Joanna, Asgari, Nasrin, Steckelings, Ulrike Muscha, and Owens, Trevor

Subjects
FOS: Clinical medicine, 111702 Aged Health Care, FOS: Health sciences, 110904 Neurology and Neuromuscular Diseases
Abstract

Supplemental material, MSJ860327_supplementary_material for Angiotensin AT2 receptor–induced interleukin-10 attenuates neuromyelitis optica spectrum disorder–like pathology by Reza Khorooshi, Emil Ulrikkaholm Tofte-Hansen, Camilla Tygesen, Roser Montanana-Rosell, Hannah Liska Limburg, Joanna Marczynska, Nasrin Asgari, Ulrike Muscha Steckelings and Trevor Owens in Multiple Sclerosis Journal

Published
2019
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15. Angiotensin AT2 receptor–induced interleukin-10 attenuates neuromyelitis optica spectrum disorder–like pathology.

Author

Khorooshi, Reza, Tofte-Hansen, Emil Ulrikkaholm, Tygesen, Camilla, Montanana-Rosell, Roser, Limburg, Hannah Liska, Marczynska, Joanna, Asgari, Nasrin, Steckelings, Ulrike Muscha, and Owens, Trevor

Subjects
NEUROMYELITIS optica, GLIAL fibrillary acidic protein, INTERLEUKIN-10, PATHOLOGY, ANGIOTENSINS, SPINAL infusions
Abstract

Background: Neuromyelitis optica spectrum disorder (NMOSD) is a relapsing inflammatory central nervous system (CNS) disease for which there is no cure. Immunoglobulin G autoantibodies specific for the water channel aquaporin-4 are a serum biomarker, believed to induce complement-dependent astrocyte damage with secondary demyelination. Objective: To investigate the effect of angiotensin AT2 receptor (AT2R) stimulation on NMOSD-like pathology and its underlying mechanism. Methods: NMOSD-like pathology was induced in mice by intracerebral injection of immunoglobulin-G isolated from NMOSD patient serum, with complement. This mouse model produces the characteristic histological features of NMOSD. A specific AT2R agonist, Compound 21 (C21), was given intracerebrally at day 0 and by intrathecal injection at day 2. Results: Loss of aquaporin-4 and glial fibrillary acidic protein was attenuated by treatment with C21. Administration of C21 induced mRNA for interleukin-10 in the brain. NMOSD-like pathology was exacerbated in interleukin-10-deficient mice, suggesting a protective role. C21 treatment did not attenuate NMOSD-like pathology in interleukin-10-deficient mice, indicating that the protective effect of AT2R stimulation was dependent on interleukin-10. Conclusion: Our findings identify AT2R as a novel potential therapeutic target for the treatment of NMOSD. Interleukin-10 signaling is an essential part of the protective mechanism counteracting NMOSD pathology. [ABSTRACT FROM AUTHOR]

Published
2020
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16. The role of metalloproteinase ADAM17 in regulating ICOS ligand-mediated humoral immune responses

Author

Marczynska Joanna, Ozga Aleksandra, Wlodarczyk Agnieszka, Majchrzak-Gorecka Monika, Kulig Paulina, Banas Magdalena, Michalczyk-Wetula Dominika, Majewski Pawel, Hutloff Andreas, Schwarz Jeanette, Chalaris Athena, Scheller Jürgen, Rose-John Stefan, and Cichy Joanna

Subjects
Male, Ovalbumin, Immunology, ADAM17 Protein, Inducible T-Cell Co-Stimulator Ligand, Mice, Immune system, Antigens, CD40, Cell surface receptor, Immunology and Allergy, Animals, CD40 Antigens, Receptor, Cells, Cultured, Mice, Knockout, B-Lymphocytes, Innate immune system, biology, Antibodies, Monoclonal, Acquired immune system, Immunoglobulin Class Switching, 3. Good health, Immunity, Humoral, ICOS LIGAND, Immunoglobulin Isotypes, Mice, Inbred C57BL, ADAM Proteins, Poly I-C, Antibody Formation, biology.protein, Female, Lymph Nodes, Antibody, Spleen
Abstract

Immune cells regulate cell surface receptor expression during their maturation, activation, and motility. Although many of these receptors are regulated largely at the level of expression, protease-mediated ectodomain shedding represents an alternative means of refashioning the surface of immune cells. Shedding is largely attributed to a family of a disintegrin and metalloprotease domain (ADAM) metalloproteases, including ADAM17. Although ADAM17 is well known to contribute to the innate immune response, mainly by releasing TNF-α, much less is known about whether/how this metalloprotease regulates adaptive immunity. To determine whether ADAM17 contributes to regulating adaptive immune responses, we took advantage of ADAM17 hypomorphic (ADAM17ex/ex) mice, in which ADAM17 expression is reduced by 90–95% compared with wild-type littermates. In this study, we show that that ADAM17 deficiency results in spleen and lymph node enlargement, as well as increased levels of Ag-specific class-switched Ig production following immunization with OVA together with anti-CD40 mAbs and polyinosinic-polycytidylic acid. Moreover, we demonstrate that the costimulatory ligand ICOS ligand (ICOSL) is selectively downregulated on the surface of B cells in an ADAM17-specific manner, although it is not proteolitically processed by recombinant ADAM17 in vitro. Finally, we show that higher cell surface levels of ICOSL in ADAM17ex/ex mice may contribute to the development of excessive Ab responses. Therefore, our data suggest a functional link between ADAM17 and ICOSL in controlling adaptive immune responses.

Published
2014

17. The Gut Microbiome Contributes to a Substantial Proportion of the Variation in Blood Lipids

Author

Fu, Jingyuan, primary, Bonder, Marc Jan, additional, Cenit, María Carmen, additional, Tigchelaar, Ettje F., additional, Maatman, Astrid, additional, Dekens, Jackie A.M., additional, Brandsma, Eelke, additional, Marczynska, Joanna, additional, Imhann, Floris, additional, Weersma, Rinse K., additional, Franke, Lude, additional, Poon, Tiffany W., additional, Xavier, Ramnik J., additional, Gevers, Dirk, additional, Hofker, Marten H., additional, Wijmenga, Cisca, additional, and Zhernakova, Alexandra, additional

Published
2015
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18. The Expression and Regulation of Chemerin in the Epidermis

Author

Banas, Magdalena, primary, Zegar, Aneta, additional, Kwitniewski, Mateusz, additional, Zabieglo, Katarzyna, additional, Marczynska, Joanna, additional, Kapinska-Mrowiecka, Monika, additional, LaJevic, Melissa, additional, Zabel, Brian A., additional, and Cichy, Joanna, additional

Published
2015
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20. Angiotensin AT2 receptor-induced interleukin-10 attenuates neuromyelitis optica spectrum disorder-like pathology.

Author

Khorooshi R, Tofte-Hansen EU, Tygesen C, Montanana-Rosell R, Limburg HL, Marczynska J, Asgari N, Steckelings UM, and Owens T

Subjects
Animals, Aquaporin 4 genetics, Autoantibodies, Humans, Interleukin-10, Mice, Neoplasm Recurrence, Local, Receptor, Angiotensin, Type 2, Neuromyelitis Optica drug therapy
Abstract

Background: Neuromyelitis optica spectrum disorder (NMOSD) is a relapsing inflammatory central nervous system (CNS) disease for which there is no cure. Immunoglobulin G autoantibodies specific for the water channel aquaporin-4 are a serum biomarker, believed to induce complement-dependent astrocyte damage with secondary demyelination., Objective: To investigate the effect of angiotensin AT2 receptor (AT2R) stimulation on NMOSD-like pathology and its underlying mechanism., Methods: NMOSD-like pathology was induced in mice by intracerebral injection of immunoglobulin-G isolated from NMOSD patient serum, with complement. This mouse model produces the characteristic histological features of NMOSD. A specific AT2R agonist, Compound 21 (C21), was given intracerebrally at day 0 and by intrathecal injection at day 2., Results: Loss of aquaporin-4 and glial fibrillary acidic protein was attenuated by treatment with C21. Administration of C21 induced mRNA for interleukin-10 in the brain. NMOSD-like pathology was exacerbated in interleukin-10-deficient mice, suggesting a protective role. C21 treatment did not attenuate NMOSD-like pathology in interleukin-10-deficient mice, indicating that the protective effect of AT2R stimulation was dependent on interleukin-10., Conclusion: Our findings identify AT2R as a novel potential therapeutic target for the treatment of NMOSD. Interleukin-10 signaling is an essential part of the protective mechanism counteracting NMOSD pathology.

Published
2020
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