Contents
Academic literature on the topic 'Immune Impact'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Immune Impact.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Dissertations / Theses on the topic "Immune Impact"
1
Warnatsch, Annika. "Impact of proteasomal immune adaptation on the early immune response to viral infection." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2013. http://dx.doi.org/10.18452/16775.
Full textAbstract:
Im Kampf gegen eine Virusinfektion spielen CD8+ T Zellen des adaptiven Immunsystems eine besondere Rolle. Sie patroullieren im Körper und entdecken spezifische Virusepitope, welche mittels MHC Klasse I Molekülen auf der Oberfläche infizierter Zellen präsentiert werden. Wird eine virus-infizierte Zelle erkannt, kann diese schnell und effizient eliminiert. Für die Generierung viraler Peptide, welche auf MHC Klasse I Komplexe geladen werden, ist das Ubiquitin-Proteasom-System von essentieller Bedeutung. Kürzlich wurden weitere Funktionen des Immunoproteasoms aufgedeckt wie zum Beispiel der Schutz gegen oxidativen Stress. Innerhalb der vorliegenden Arbeit konnte die Fähigkeit des Immunoproteasoms gegen eine Akkumulation oxidativ geschädigter Proteine zu schützen mit der Generierung von MHC Klasse I Liganden kombiniert und neu interpretiert werden. Es konnte gezeigt werden, dass während einer Virusinfektion in Nicht-Immunzellen die Produktion reaktiver Sauerstoffspezies durch die alternative NADPH Oxidase Nox4 eine bedeutende Rolle spielt. Die Aktivierung von Nox4 resultiert in der Akkumulation oxidativ geschädigter Proteine. Innerhalb von zwei Stunden nach dem Eintreten von Viruspartikeln in die Zellen wurden strukturelle Virusproteine oxidiert und anschließend ubiquityliert. Die gleichzeitige, virus-induzierte Expression von Immunoproteasomen führte zu einem schnellen und effizienten Abbau ubiquitylierter Virusantigene. Infolgedessen konnten immundominante Virusepitope vermehrt freigesetzt werden. Folglich wurde ein soweit unbekannter Mechanismus gefunden, welcher Substrate für das Proteasom zur Generierung von MHC Klasse I Liganden bereitstellt. Zusammenfassend konnte innerhalb dieser Arbeit gezeigt werden, dass das Immunoproteasom den Schutz vor oxidativen Stress mit der Generierung antigener Peptide verbindet, wodurch eine effektive adaptive Immunantwort etabliert werden kann.<br>An efficient immune control of virus infection is predominantly mediated by CD8+ T cells which patrol through the body and eliminate infected cells. Infected cells are recognized when they present viral antigenic peptides on their surface via MHC class I molecules. To make antigenic peptides available for loading on MHC class I complexes, the ubiquitin proteasome system plays a crucial role. Moreover, the induction of the i-proteasome is known to support the generation of MHC class I ligands. Recently, new functions of the i-proteasome have been discovered. Evidence is increasing that the i-proteasome is involved in the protection of cells against oxidative stress. Within this thesis the characteristic of the i-proteasome to protect cells against the accumulation of oxidant-damaged proteins could be linked to its role in improving the generation of MHC class I ligands. It could be demonstrated that during a virus infection in non-immune cells the production of reactive oxygen species by the alternative NADPH oxidase Nox4 is of critical importance resulting in the accumulation of potentially toxic oxidant-damaged proteins. Indeed, within two hours of infection structural virus proteins were oxidized and subsequently poly-ubiquitylated. The concomitant formation of i-proteasomes led to a rapid and efficient degradation of ubiquitylated virus antigens thereby improving the liberation of immunodominant viral epitopes. In conclusion, a so far unknown mechanism to fuel proteasomal substrates into the MHC class I antigen presentation pathway has been revealed. A new protein pool consisting of exogenously delivered viral proteins provides proteasomal substrates in the very early phase of a virus infection. Within the scope of this thesis the i-proteasome has been shown to link the protection against oxidative stress, initiated directly by pathogen recognition, with the generation of antigenic peptides. Together, an effective adaptive immune response is triggered.
2
Kühl, Thomas. "Pathogenic impact of immune-related cells in Batten disease." Thesis, King's College London (University of London), 2012. https://kclpure.kcl.ac.uk/portal/en/theses/pathogenic-impact-of-immunerelated-cells-in-batten-disease(ff86b71b-e859-4d91-a378-421eab71ae97).html.
Full textAbstract:
The neuronal ceroid lipofuscinoses (NCLs or Batten disease) are inherited neurodegenerative diseases of children. In all types of NCL glial activation, the innate immune response of the brain, precedes neurodegeneration. However, it is unclear whether adaptive immune responses are also involved in these diseases, or if they directly contribute to disease pathogenesis. Therefore, we examined the role of adaptive immune cells in mouse models of Infantile NCL (Ppt1-/- mice) and Juvenile NCL (Cln3-/- mice) by identifying, localising, and subsequently genetically removing immune components. Characterising the adaptive immune response within Ppt1-/- and Cln3-/- mice, we revealed evidence for progressive CNS infiltration by different classes of T-cells in both forms of NCL. To analyse the pathogenic impact of these lymphocytes, we crossbred PptP/- mutants with mice deficient in Rag-1, which lack T- and B-lymphocytes. Disease progression was significantly delayed in immune deficient PptP/ /Rag-1-/- mice, which displayed ameliorated neuroinflammation and neuron loss. We also crossed our Infantile and Juvenile NCL mouse models with mice deficient in sialoadhesin (Sn), a binding protein found on macrophages and microglia, and is involved in pro-inflammatory T-cell regulation. Disease progression was also slowed down, with significantly increased neuron survival in both Sn deficient NCL mice. However, contrasting effects on glial activation were observed between Ppt1~/-/ ’ Sn~/-and Cln3-/-/Sn-/- mice. Whereas glial activation was only marginally attenuated in Cln3-/-/Sir/- mice, significantly decreased microglial activation and enhanced astrocytosis were observed in Ppt1-/-/Str/- mice. These latter findings suggest an unexpected link between macrophage-expressed Sn and astrocytosis in Taken together, our findings prove that adaptive immune cells and sialoadhesin each appear to contribute to disease progression in Infantile and Juvenile NCL mice. Therefore, both immune components could prove to be suitable therapeutic targets for these fatal disorders.
3
Post, Frank A. "Mycobacterial strain diversity : impact on the host immune response." Doctoral thesis, University of Cape Town, 2003. http://hdl.handle.net/11427/2717.
Full text
4
Zhao, Wei. "Impact of the innate immune response on mammary epithelia." [Ames, Iowa : Iowa State University], 2009.
Find full text
5
Daniłowicz-Luebert, Emilia. "Impact of helminths and helminth products on immune responses." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2013. http://dx.doi.org/10.18452/16683.
Full textAbstract:
Helmintheninfektionen induzieren in ihren Wirten Typ 2 (Th2) Immunantworten, welche parasitäre Larvenstadien hemmen und/oder zur Abstoßung von intestinalen Würmern führen. Th2-Antworten können auch gegenüber Umweltallergenen ausgebildet werden und allergische Reaktionen vermitteln. Mastzellen (MZ) spielen eine herausragende Rolle für die Wirtsantwort gegen Parasiten. Die Ergebnisse der vorliegenden Arbeit zeigen, dass eine Infektion von MZ-defizienten Mäusen mit Helminthen zu einer reduzierten Produktion von IL-25, IL-33 und TSLP, einer beeinträchtigten Etablierung von Th2 Immunantworten und einer erhöhten Wurmlast führt. Diese Parameter konnten allerdings nach einem erfolgreichen Transfer von Knochenmark aus Wildtypmäusen wiederhergestellt werden. Die vorliegende Arbeit beschreibt somit eine wichtige Funktion von Mastzellen für die Initialisierung von Th2 Immunantworten. Des Weiteren konnte gezeigt werden, dass ein Cystein-Protease-Inhibitor - AvCystatin sowohl Parameter von Atemwegsentzündung und -hyperreaktivität als auch Lieschgraspollen (Phl p 5b)-spezifische Immunantworten in einem klinisch relevanten Mausmodell für Atemwegsentzündung inhibiert. Gleichzeitig führte die Behandlung mit AvCystatin zu einem Anstieg von IL-10 und erhöhten Frequenzen von CD4+CD25+Foxp3+ T Zellen. Die in vivo Effekte von AvCystatin wurden unabhängig von der Protease-inhibitorischen Aktivität des Immunmodulators oder dessen Fähigkeit zur Oligomerisation vermittelt. AvCystatin unterdrückte zudem die Allergen-spezifische Produktion von IL-13 und induzierte in vitro unter Verwendung mononukleärer Zellen aus dem peripheren Blut (PBMCs) von Graspollen allergischen Patienten einen IFN-gamma vermittelten Th1 shift. Zusammenfassend tragen die Ergebnisse der Arbeit zu einem besseren Verständnis für die frühen Ereignisse von Th2 Immunantworten bei und zeigen, dass Helminthenmoleküle Bystandereffekte auf Immunantworten vermitteln können, die gegen andere Antigene gerichtet sind.<br>Helminth infections induce protective type 2 (Th2) immune responses in the host leading to arrested larval development and/or intestinal worm expulsion. Moreover, Th2 immune responses are initiated against harmless environmental allergens and mediate development of allergic disease. Among multiple mechanisms implicated in host responses to parasites and allergens, mast cells (MCs) play a pivotal role. The present study shows that MC-deficient mouse strains following infection with two gastrointestinal helminths had dramatically reduced early production of the tissue-derived cytokines IL-25, IL-33, and TSLP, which resulted in impaired induction of Th2 immune responses as well as increased parasite burden. These parameters were restored after transfer of WT bone marrow. These data reveal an important role for MCs in orchestrating type 2 immune responses. Parasites have developed various strategies to modulate the immune system via induction of a range of regulatory mechanisms. In this study AvCystatin, the filarial cysteine inhibitor, was found to inhibit airway inflammation and hyperreactivity induced by a clinically relevant allergen of timothy grass pollen (Phl p 5b). AvCystatin increased levels of the regulatory cytokine IL-10 and total numbers of CD4+CD25+Foxp3+ T cells. The immunomodulatory effect in vivo was found to be independent of AvCystatin’s protease inhibitor activity or oligomerization. Finally, AvCystatin suppressed allergen-specific production of IL-13 and created a shift towards Th1 immunity by increased levels IFN-gamma of human peripheral blood mononuclear cells (PBMCs) from grass pollen allergic patients. The findings contribute to a better understanding of the early events that dictate the priming of type 2 immune responses. Furthermore, helminth product-induced suppression may also have effects on bystander responses to unrelated antigens, thus, suggesting a promising preventive and therapeutic concept in the treatment of aberrant inflammations.
6
Blaimer, Stephanie [Verfasser], and Edward K. [Akademischer Betreuer] Geissler. "Impact of innate and adaptive immune cells in tumor immune surveillance / Stephanie Blaimer ; Betreuer: Edward K. Geissler." Regensburg : Universitätsbibliothek Regensburg, 2020. http://d-nb.info/1210729202/34.
Full text
7
Banerjee, Piu. "Immune mechanisms in atopic eczema and the impact of therapy." Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.391635.
Full text
8
Pike, Lewis James. "Salmonella vaccines : the impact of antigenic location on immune responses." Thesis, University of York, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.313867.
Full text
9
Weaver, Wade G. "Impact of VHSV M Protein on the Innate Immune System." University of Toledo / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1481191320713471.
Full text
10
Howells, Anwen. "The impact of innate immune cells on immunopathology in dengue." Thesis, University of Oxford, 2014. https://ora.ox.ac.uk/objects/uuid:0a251372-4d0e-416d-ad3c-8e07e6729e1b.
Full textAbstract:
Dengue virus (DENV) is an arthropod-borne virus and has become a worldwide problem with steadily rising annual infection rates. Patients present with a range of symptoms from mild fever to, in some cases, life-threatening hemorrhagic fever and shock syndrome. The most severe cases require emergency hospital care and currently, there is no effective drug treatment or vaccine for dengue. As severe symptoms appear post-peak viremia, immuno-pathology is thought to be the cause and a potential trigger of this is differential activation of the immune response upon recognition of DENV. This could be due to a combination of factors including varying receptors, signalling pathways and immune regulation mechanisms. In order to understand DENV infection better, it is imperative to study the mechanisms of activation and control of immune responses triggered by the virus. Very early events in viral infection (after 10 min stimulation) were studied aiming to identify proteins involved in differential activation of immune responses. Phosphorylated proteins were isolated from cells post-stimulation and analysed by mass spectrometry. More than 200 proteins were differentially regulated by phosphorylation in response to DENV stimulation as compared to Mock, Influenza A virus and LPS stimulation. The effect of two specific proteins, namely Calpain-2 and Importin-5, identified to be differentially phosphorylated was investigated further. Calpain-2 was seen to be vital in the efficient production of progeny virions and the transcription of Mx1, an anti-viral interferon stimulated gene. Importin-5 is known to transport DENV NS5 into the nucleus during infection and was seen to co-precipitate with many host proteins. In summary, it is imperative that novel treatments and vaccines are developed for dengue as it is one of the worldâs most prevalent arthropod-borne viruses. It was discovered here that many proteins undergo phosphorylation/de-phosphorylation in response to DENV stimulation to a differing degree than other stimuli. Calpain-2 plays a vital role DENV infection, potentially influencing the potency of immune response. Importin-5 associates with various host proteins during DENV infection, potentially altering their function or the function of Importin-5 itself. Research into targeted inhibition of Calpain-2 function or Importin-5 interaction with DENV NS5 could lead to a successful anti-viral treatment for DENV infection.