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26 results on '"Klaska, Izabela"'

3. Dendritic cell-based therapy of experimental autoimmune uveoretinitis

Author

Klaska, Izabela

Subjects
610, Uveitis, Dendritic cells, Eye
Abstract

Recently, there has been considerable interest in developing specific cell-based immunotherapies using dendritic cells (DCs). Here the mechanisms underlying the tolerogenic properties of DCs in the suppression of experimental autoimmune uveoretinitis (EAU), the mouse model of human sight threatening autoimmune uveitis, were examined. Immature DCs have the ability to promote immune tolerance to self antigens and to prevent the development of autoimmune disorders including EAU. However there is a risk that immature DCs placed in the inflammatory environment would undergo maturation and instead of tolerance promote immunity. Therefore much effort has been directed to develop protocols that stabilize the tolerogenic DC properties which would ultimately ensure safety and effectiveness of DC-based vaccines. Previous work demonstrated that activation of DCs with lipopolysaccharide (LPS) increases the ability of these cells to prevent EAU. Here, it was demonstrated that LPS promotes the activation of both TRIF and MyD88 signalling pathways in DCs which after 24 h LPS treatment secreted a significant amount of IL-10, IFN-β, IL-1β, IL-6 and TNF-α while the level of secreted IL-12 is low. It was further shown that LPSinduced enhancement of the tolerogenic properties of DCs correlates with the state of endotoxin tolerance in the DCs, rendering them refractory to further stimulation. It was hypothesised that the LPS-induced enhancement of DC tolerogenicity is due to the reduced expression of the TLR4, which subsequently disables several signalling pathways and prevent DCs from initiating adaptive T cell immunity. In summary, the presented data provides valuable insights into the mechanisms involved in the suppression of autoimmune uveitis using a DC-based therapy.

Published
2013

9. Intravitreal administration of recombinant human opticin protects against hyperoxia-induced pre-retinal neovascularization

Author

Klaska, Izabela P., primary, White, Anne, additional, Villacampa, Pilar, additional, Hoke, Justin, additional, Hervás, Laura A., additional, Maswood, Ryea N., additional, Ali, Robin R., additional, Bunce, Catey, additional, Unwin, Richard D., additional, Cooper, Garth J.S., additional, Bishop, Paul N., additional, and Bainbridge, James W., additional

Published
2021
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12. Treatment With FoxP3+ Antigen-Experienced T Regulatory Cells Arrests Progressive Retinal Damage in a Spontaneous Model of Uveitis

Author

Liu, Yi-Hsia, primary, Mölzer, Christine, additional, Makinen, Kimmo, additional, Kamoi, Koju, additional, Corbett, Clare L. C., additional, Klaska, Izabela P., additional, Reid, Delyth M., additional, Wilson, Heather M., additional, Kuffová, Lucia, additional, Cornall, Richard J., additional, and Forrester, John V., additional

Published
2020
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14. Stabilization of myeloid-derived HIFs promotes vascular regeneration in retinal ischemia

Author

Villacampa, Pilar, primary, Liyanage, Sidath E., additional, Klaska, Izabela P., additional, Cristante, Enrico, additional, Menger, Katja E., additional, Sampson, Robert D., additional, Barlow, Maeve, additional, Abelleira-Hervas, Laura, additional, Duran, Yanai, additional, Smith, Alexander J., additional, Ali, Robin R., additional, Luhmann, Ulrich F. O., additional, and Bainbridge, James W. B., additional

Published
2019
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15. Neonatal brain-directed gene therapy rescues a mouse model of neurodegenerative CLN6 Batten disease

Author

kleine Holthaus, Sophia-Martha, primary, Herranz-Martin, Saul, additional, Massaro, Giulia, additional, Aristorena, Mikel, additional, Hoke, Justin, additional, Hughes, Michael P, additional, Maswood, Ryea, additional, Semenyuk, Olha, additional, Basche, Mark, additional, Shah, Amna Z, additional, Klaska, Izabela P, additional, Smith, Alexander J, additional, Mole, Sara E, additional, Rahim, Ahad A, additional, and Ali, Robin R, additional

Published
2019
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16. Neonatal brain-directed gene therapy rescues a mouse model of neurodegenerative CLN6 Batten disease

Author

Holthaus, Sophia-Martha kleine, primary, Martin-Herranz, Saul, additional, Massaro, Giulia, additional, Aristorena, Mikel, additional, Hoke, Justin, additional, Hughes, Michael P., additional, Maswood, Ryea, additional, Semenyuk, Olha, additional, Basche, Mark, additional, Shah, Amna Z., additional, Klaska, Izabela P., additional, Smith, Alexander J., additional, Mole, Sara E., additional, Rahim, Ahad A, additional, and Ali, Robin R, additional

Published
2019
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22. A Role for PP1/NIPP1 in Steering Migration of Human Cancer Cells

Author

Martin-Granados, Cristina, primary, Prescott, Alan R., additional, Van Dessel, Nele, additional, Van Eynde, Aleyde, additional, Arocena, Miguel, additional, Klaska, Izabela P., additional, Görnemann, Janina, additional, Beullens, Monique, additional, Bollen, Mathieu, additional, Forrester, John V., additional, and McCaig, Colin D., additional

Published
2012
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23. Mouse Models of Autoimmune Uveitis

Author

P. Klaska, Izabela and V. Forrester, John

Abstract

Uveitis is a sight threatening intraocular inflammation accounting for approximately 10% of blindness worldwide. On the basis of aetiology, disease can be classified as infectious or non-infectious; and by anatomical localization of inflammation as anterior, posterior and panuveitis. Non-infectious uveitis is believed to be autoimmune in nature with Th1 and Th17 cells being identified as the prominent effector cell types. Numerous animal models of autoimmune uveitis were developed contributing to our understanding of this inflammatory condition. The classical peptide-induced experimental autoimmune uveoretinitis (EAU) model resembles human posterior uveitis due to the recurrent/relapsing nature of the disease; while the intraocular inflammation triggered by administration of bacterial lipopolisaccharide (endotoxin-induced uveitis, EIU) mimics closely anterior uveitis. The clinical need for novel, more targeted forms of anti-inflammatory therapy has emerged as currently available therapeutic strategies are associated with a number of adverse effects and intolerance in patients. This review summarises knowledge about existing mouse models of uveitis, discusses mechanisms driving intraocular inflammation and describes possible customised translational treatment strategies that can be potentially used in the clinic to prevent blindness in patients.

Published
2015

25. Effects of PEDF and VEGF on PACAP-/VIP-induced cAMP formation in rat brain derived astrocyte cultures.

Author

Klaska I, Bednarek K, and Nowak JZ

Subjects
Animals, Astrocytes metabolism, Brain metabolism, Cells, Cultured, Dose-Response Relationship, Drug, Humans, Pituitary Adenylate Cyclase-Activating Polypeptide antagonists & inhibitors, Rats, Rats, Wistar, Vasoactive Intestinal Peptide antagonists & inhibitors, Astrocytes drug effects, Brain drug effects, Cyclic AMP biosynthesis, Eye Proteins pharmacology, Nerve Growth Factors pharmacology, Pituitary Adenylate Cyclase-Activating Polypeptide pharmacology, Serpins pharmacology, Vascular Endothelial Growth Factor A pharmacology, Vasoactive Intestinal Peptide pharmacology
Abstract

Pituitary adenylate cyclase-activating polypeptide (PACAP) and vasoactive intestinal peptide (VIP) are two structurally related peptides acting on their specific receptors. Both were shown to concentration-dependently (0.001 nM - 1 muM) stimulate cyclic 3',5' adenosinomonophosphate (cAMP) formation in rat primary glial cell (astrocyte) cultures, with PACAP being distinctly more potent than VIP. The acute effects of the peptides were significantly suppressed (25% and 36% for PACAP and VIP, respectively) when tested in cell cultures preincubated for 24 h (but not 2 h) in the presence of pigment epithelium-derived factor (PEDF, 50 ng/ml). Both 24 h and 2 h preincubation of cells with vascular endothelial growth factor (VEGF, 50 ng/ml) had no influence on PACAP or VIP actions. The addition of PEDF and VEGF together for 24 h preincubation, produced suppression of the PACAP- or VIP-evoked cAMP responses similar to that seen with PEDF alone. Neither PEDF nor VEGF significantly affected cAMP generation in an assay with a 15-min incubation, which is a standard incubation period for PACAP and VIP. The findings show that PEDF, displaying by itself no effect on cAMP generating system in rat astrocytes, significantly affected biological activity of both PACAP and VIP. The reported observation may be of significance, considering the neurotrophic and/or neuroprotective activity of the tested polypeptides.

Published
2008

26. [The role of complement in physiology and pathology].

Author

Klaska I and Nowak JZ

Subjects
Animals, Complement Activation physiology, Complement Factor H chemistry, Complement Inactivator Proteins physiology, Complement Membrane Attack Complex chemistry, Complement Pathway, Alternative physiology, Complement System Proteins chemistry, Glomerulonephritis, Membranoproliferative immunology, Glomerulonephritis, Membranoproliferative pathology, Hemolytic-Uremic Syndrome immunology, Hemolytic-Uremic Syndrome pathology, Humans, Macular Degeneration immunology, Macular Degeneration pathology, Complement C3 Convertase, Alternative Pathway physiology, Complement Factor H physiology, Complement Membrane Attack Complex physiology, Complement System Proteins physiology, Glomerulonephritis, Membranoproliferative metabolism, Hemolytic-Uremic Syndrome metabolism, Macular Degeneration metabolism
Abstract

The complement system was discovered over one hundred years ago. It is an essential part of the innate immune system. A group of about 40 proteins assists in phagocytosis and stimulates inflammation. The complement system participates in the defense of an organism against different factors, e.g. microorganisms. There are three pathways of complement activation: the classical, lectin, and alternative. Activation of the complement system leads to the formation of a lytic macromolecule known as the membrane attack complex (MAC). The MAC may damage target cells in a process called bacteriolysis. The host organism is protected against the negative impact of autoimmunity by complement factor H (CFH). Recent experimental studies dealing with the regulation of the complement system suggest that this control process can be genetically determined. Mutations in genes encoding CFH (CFH polymorphism), factor B, and C2, can be crucial for a defective or insufficient regulation of the complement system. This paper surveys recent achievements on the structure and mechanisms of the complement system and shortly reviews the correlation between the complement function and pathogenesis of many diseases, including atypical hemolytic uremic syndrome (aHUS), membranoproliferative glomerulonephritis II (MPGN II), and age-related macular degeneration (AMD).

Published
2007

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