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Dissertations / Theses on the topic 'Type I interferon pathway'

Author: Grafiati

Published: 4 June 2021

Last updated: 2 February 2022

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1

Liu, Qinfang. "Interaction of type I interferons and mTOR signaling underlying PRRSV infection." Thesis, Kansas State University, 2016. http://hdl.handle.net/2097/32860.

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Master of Science in Biomedical Sciences<br>Department of Anatomy and Physiology<br>Yongming Sang<br>Animal metabolic and immune systems integrate and inter-regulate to exert effective immune responses to distinct pathogens. The signaling pathway mediated by mechanistic target of rapamycin (mTOR) is critical in cellular metabolism and implicated in host antiviral responses. Recent studies highlight the significance of the mTOR signaling pathway in the interferon (IFN) response. Type I IFNs mediate host defense, particularly, against viral infections, and have myriad roles in antiviral innate a

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2

Qin, Zhihua. "SAMHD1 Negatively Regulates the Innate Immune Responses to Inflammatory Stimuli and Viral Infection." The Ohio State University, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=osu1587587968104986.

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3

Barnabei, Laura. "New genetic predisposition to early-onset autoimmunity in human : implication of the NF-κB pathway Heterozygous RELA mutations cause early-onset systemic lupus erythematosus by hijacking the NFkB pathway towards transcriptional activation of type-I Interferon promoter". Thesis, Sorbonne Paris Cité, 2019. http://www.theses.fr/2019USPCB049.

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Le lupus érythémateux systémique (LES) est une maladie auto-immune et inflammatoire caractérisée par une production excessive d'auto-anticorps et de cytokines pro-inflammatoires, notamment l'interféron de type 1. Afin d'identifier de nouveaux facteurs génétiques associés au LES, un whole exome sequencing (WES) nous a permis d'identifier deux mutations différentes du gène RELA chez 3 patients LES ayant débuté à l'âge adulte ou pédiatrique. RELA code la protéine p65 qui est une sous-unité du facteur de transcription NF-κB. Les mutations retrouvées H86N et R329X de RELA conduisent à l'activation

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4

Miyahira, Andrea Kiem Hwa Malawaina. "The regulation of type I interferon responses to pathogen recognition receptor pathways by TANK-binding kinase-1." Diss., Restricted to subscribing institutions, 2008. http://proquest.umi.com/pqdweb?did=1693160891&sid=7&Fmt=2&clientId=1564&RQT=309&VName=PQD.

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5

Wang, Ling, and Shunbin Ning. ""Toll-Free" Pathways for Production of Type I Interferons." Digital Commons @ East Tennessee State University, 2017. https://dc.etsu.edu/etsu-works/6540.

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Pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs) are recognized by different cellular pathogen recognition receptors (PRRs), which are expressed on cell membrane or in the cytoplasm of cells of the innate immune system. Nucleic acids derived from pathogens or from certain cellular conditions represent a large category of PAMPs/DAMPs that trigger production of type I interferons (IFN-I) in addition to pro-inflammatory cytokines, by specifically binding to intracellular Toll-like receptors or cytosolic receptors. These cytosolic receptors, which are

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6

Ghislain, Julien Johannes. "Type I interferon signal transduction." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0015/NQ27652.pdf.

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7

Fenner, Jennifer Eve. "Regulation of Type I interferon responses." Monash University, Centre for Functional Genomics and Human Disease, 2003. http://arrow.monash.edu.au/hdl/1959.1/9437.

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8

Kamphuis, Elisabeth. "Type I interferon stimulation of lymphocytes." Giessen : VVB Laufersweiler, 2007. http://geb.uni-giessen.de/geb/volltexte/2007/4791/index.html.

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9

Kamphuis, Elisabeth. "Type I interferon stimulation of lymphocytes." Giessen VVB Laufersweiler, 2006. http://d-nb.info/988717891/34.

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10

Hidmark, Åsa. "Induction of type I interferons and viral immunity /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-227-9/.

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11

Limmer, Kirsten. "Mechanisms of regulation in the interferon factor 3 (IRF-3) pathway." Diss., [La Jolla, Calif.] : University of California, San Diego, 2008. http://wwwlib.umi.com/cr/ucsd/fullcit?p3336510.

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Thesis (Ph. D.)--University of California, San Diego, 2008.<br>Title from first page of PDF file (viewed Jan. 5, 2009). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references.

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12

Blanc, Mathieu. "Sterol biosynthesis pathway is part of the interferon host defence response." Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/5556.

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Recently, cholesterol metabolism has been shown to modulate the infection of several viruses and there is growing evidence that inflammatory response to infection also modulates lipid metabolism. However little is known about the role of inflammatory processes in modulating lipid metabolism and their consequences for the viral infection. This study investigates host-lipid viral interaction pathways using mouse cytomegalovirus, a large double-stranded DNA genome, which represents one of the few models for a natural infection of its natural host. In this study, transcriptomic and lipidomic profi

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13

Walker, Angela Marie Roberts R. M. "The type I IFN of Bos taurus." Diss., Columbia, Mo. : University of Missouri-Columbia, 2008. http://hdl.handle.net/10355/6864.

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The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Title from PDF of title page (University of Missouri--Columbia, viewed on April 1, 2010). Vita. Thesis advisor: R. Michaels Roberts. "May 2008" Includes bibliographical references

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14

Lövgren, Tanja. "Endogenous Type I Interferon Inducers in Systemic Autoimmune Diseases." Doctoral thesis, Uppsala University, Department of Medical Sciences, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-7181.

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<p>Patients with systemic lupus erythematosus (SLE) have elevated levels of interferon (IFN)-α in blood and IFN-α-producing cells in tissues. In the present thesis, we investigate the mechanisms behind the upregulated IFN-α-production in SLE and also show that the IFN-α system is activated in primary Sjögren’s syndrome (pSS), with IFN-α-producing cells in the major affected organ, the salivary glands. The IFN-α is a type I IFN, a family of cytokines counteracting especially viral infections, by acting directly on infected cells, and via many immunomodulatory effects. The latter may also contri

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15

Lövgren, Tanja. "Endogenous type I interferon inducers in systemic autoimmune diseases /." Uppsala : Acta Universitatis Upsaliensis, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-7181.

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16

Bazzigher, Luigi G. "Interferon-induced Mx proteins /." Zürich, 1992. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=9650.

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17

Kew, Chun, and 喬駿. "Inhibition of PACT mediated type 1 interferon production by herpes simplex virus type 1 Us11 protein." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/206481.

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Mammals have complicated antiviral innate immunity to combat viral infection and this poses a strong selection pressure on the viruses. As a result, many viruses have evolved different strategies to disrupt the function of hosts’ antiviral innate immunity. Herpes simplex virus type 1 (HSV-1) is one of the examples. HSV-1 is a common and important human pathogen. HSV-1 infection induces type I interferons (IFNs) which restrict viral replication potently. To ensure persistent infection and successful replication, HSV-1 encodes several IFN-suppressing proteins. One example is Us11. Interaction be

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18

Jones, Meleri. "Interfering with interferon : developing a reporter system to study the interaction between hepatitus C viral proteins and the interferon signalling pathway." Thesis, Queen Mary, University of London, 2008. http://qmro.qmul.ac.uk/xmlui/handle/123456789/1530.

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The aim of the project was to investigate the mechanism by which HCV evades therapeutic IFN treatment. This involved the development of novel testing systems and their application to patient samples. Initial experiments focused on flavivirus replicons and novel observations on effects of one of these replicons (dengue virus) on interferon signalling were made. The dengue replicon system was demonstrated to inhibit IFNa signalling by reducing the expression of STAT2, an essential component of the type I IFN signalling pathway. This phenomenom was then further examined in dengue virus infected h

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19

Sabourighannad, Masoud. "Molecular biology of hepatitis C virus : interactions with the interferon-beta signalling pathway." Thesis, University of Leeds, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.423006.

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20

Lincez, Pamela Joan. "MDA5 and a type 1 interferon signature in the development of type 1 diabetes." Thesis, University of British Columbia, 2015. http://hdl.handle.net/2429/52850.

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Type 1 diabetes (T1D) is a debilitating disease involving the autoimmune destruction of insulin-producing pancreatic β-cells. The personal and economic burden of this disease is enormous, therefore simpler and more cost effective therapeutic approaches than those currently available must be explored. In children at risk for T1D, a unique type 1 interferon (IFN-I) transcriptional signature precedes islet autoimmunity. Recent onset of T1D strongly associates with infection by RNA viruses like coxsackievirus that induce IFN-I. Importantly, genetic variants in the T1D risk locus IFIH1 are linked

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21

Barchet, Winfried. "Cellular origin and molecular expression mechanisms of virus-induced type I interferon in vivo." [S.l. : s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=964889234.

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22

Kamphuis, Elisabeth [Verfasser]. "Type I interferon stimulation of lymphocytes / eingereicht von Elisabeth Kamphuis." Giessen : VVB Laufersweiler, 2007. http://d-nb.info/988717891/34.

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23

Huerga, Encabo Hector 1989. "Analysis of transcription mechanisms that limit type I interferon responses." Doctoral thesis, Universitat Pompeu Fabra, 2018. http://hdl.handle.net/10803/666035.

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24

Ng, Ming-him, and 吳明謙. "Negative regulation of type-I interferon production by MIP-T3." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B43572212.

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25

Ng, Ming-him. "Negative regulation of type-I interferon production by MIP-T3." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B43572212.

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26

Thibault, Donna lynn. "Type I interferon in the pathogenesis of systemic lupus erythematosus /." May be available electronically:, 2007. http://proquest.umi.com/login?COPT=REJTPTU1MTUmSU5UPTAmVkVSPTI=&clientId=12498.

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27

Liu, Yi. "Negative Regulation of Type I Interferon Induction in Dendritic Cells." Case Western Reserve University School of Graduate Studies / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=case1310149509.

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28

Slater, Louise. "Regulation of human rhinovirus induced type I interferon-β, type III interferon-λ and pro-inflammatory cytokine gene expression in normal human bronchial epithelial cells". Thesis, Imperial College London, 2008. http://hdl.handle.net/10044/1/4404.

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Asthma is an economically important disease, with exacerbations causing significant morbidity and morality. Viral infections cause ~80% of asthma exacerbations; the majority of which are attributed to rhinovirus infection. How rhinovirus infection leads to an acute asthma exacerbation is incompletely understood. The up-regulation of proinflammatory cytokines/chemokines from rhinovirus infected bronchial epithelial cells and an impaired ability of rhinovirus infected asthmatic bronchial epithelial cells to produce type I interferon-β and type III interferon-λs, are believed to contribute. This

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29

Lu, Jennifer. "Interferon-induced transmembrane proteins inhibit human immunodeficiency virus type 1 replication." Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=95120.

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Viral infection triggers production of interferon (IFN) that in turn leads to the expression of genes known as IFN-stimulated genes (ISGs), some of which possess antiviral activities. Previous studies have shown that IFN suppresses the replication of human immunodeficiency virus type I (HIV-1). While several ISGs have been linked to this specific antiviral activity with well-defined inhibitory mechanisms, others remain to be investigated. With the purpose of identifying novel ISGs capable of inhibiting HIV-1 replication, we have performed a shRNA screen of the genes upregulated by IFN in SupT1

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30

Wright, Jordan. "The role of PML proteins in adenovirus type 5 infection and the type I interferon response." Thesis, University of Warwick, 2010. http://wrap.warwick.ac.uk/3828/.

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Promyelocytic leukaemia (PML) proteins consist of a collection of related isoforms that are the nucleating components of sub-nuclear structures termed PML nuclear bodies (PML NBs). Numerous functions are attributed to PML and PML NBs, including a role in antiviral responses. Adenovirus type 5 (Ad5) has previously been shown both to disrupt PML NBs and to cause the appearance of a novel PML protein species, termed PML-A, in a manner dependent on the viral E4 Orf3 protein. Here, the interactions between Ad5 and PML proteins were further investigated. The E4 Orf3-dependent species of PML (PML-A)

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31

Pervolaraki, Kalliopi [Verfasser], and Steeve [Akademischer Betreuer] Boulant. "Functional differences in type I versus type III interferon mediated immunity / Kalliopi Pervolaraki ; Betreuer: Steeve Boulant." Heidelberg : Universitätsbibliothek Heidelberg, 2018. http://d-nb.info/1177044250/34.

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32

Wunderlich, Andrea [Verfasser]. "Direct regulation of the interferon signaling pathway by the bromodomain containing protein 4 / Andrea Wunderlich." Berlin : Freie Universität Berlin, 2013. http://d-nb.info/1037726030/34.

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33

Call, Richard. "EXAMINATION OF NAK-ASSOCIATED PROTEIN-1 (NAP1) HOMO AND HETERO-INTERACTIONS IN THE INTERFERON PATHWAY”." VCU Scholars Compass, 2011. http://scholarscompass.vcu.edu/etd/2502.

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Double stranded RNA (dsRNA), the genomic material of some viruses and a replication intermediate in others, is recognized by multiple signaling receptors that initiate the anti-viral response1. Viruses have developed mechanisms to circumvent the anti-viral response by targeting components of the signaling pathway. An example of one such pathway is the TLR3 signaling pathway, which contains a kinase complex that activates interferon regulatory factor 3 (IRF3), leading to production of type I interferons. The kinase complex consists of a scaffold protein, NAK-associated protein 1 (NAP1), a

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34

Parker, Nadeene. "The characterisation of a novel type-1 interferon-induced gene in mice." Thesis, Imperial College London, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.401715.

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35

Riding, Rebecca L. "The Role of Type I Interferon in Vitiligo Pathogenesis and Melanoma Immunotherapy." eScholarship@UMMS, 2020. https://escholarship.umassmed.edu/gsbs_diss/1065.

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Vitiligo is an autoimmune skin disease in which the pigment producing cells of the epidermis, melanocytes, are targeted for destruction by CD8+ T cells specific for melanocyte/melanoma-shared antigens. Previous work has identified IFNg as the central cytokine driving disease pathogenesis in both human patients and in our mouse model of vitiligo. IFNg signaling induces production of the chemokines CXCL9 and CXCL10, which trigger autoreactive T cell migration into the epidermis where effector T cells can target and destroy melanocytes. However, both IFNg and type I IFN signaling through activati

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36

Wiens, Kirsten E. "Type I Interferon Induction by Diverse Strains of the Mycobacterium Tuberculosis Complex." Thesis, New York University, 2017. http://pqdtopen.proquest.com/#viewpdf?dispub=10249580.

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<p> Bacterial strains from the <i>Mycobacterium tuberculosis</i> complex (MTBC) are functionally diverse and vary in both geographic distribution and potential to cause tuberculosis (TB) disease. <i>Mycobacterium africanum </i>—a lineage of the MTBC—is restricted to West Africa and causes slower progression to active tuberculosis (TB) after initial infection than other MTBC lineages. We hypothesized that this may be partly due to how bacterial strains from these lineages interact with the host immune response. Specifically, we predicted that <i>M. africanum</i> would induce less of

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37

Balman, Elizabeth Philippa. "Investigation of type-I interferon regulated gene expression in murine dendritic cells." Thesis, University College London (University of London), 2006. http://discovery.ucl.ac.uk/1445305/.

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Dendritic cells (DCs) provide a vital link between the innate and adaptive immune systems, allowing for detection of invading pathogens and the rapid initiation of an appropriate response. Until recently, research on type-I interferons (IFN-I) has focused on their function as viral inhibitors. However, it is now evident that IFN-I also has multiple roles in immune regulation, including the alteration of DC function. IFN-I has been shown to enhance T and B cell responses in vivo through stimulation of DCs, but the mechanisms by which IFN-I acts on DCs to produce these effects are unclear. We ha

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38

Millward, Jason Michael 1976. "Interferon-gamma and the regulation of neuroinflammation." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=115699.

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Inflammation of the central nervous system (CNS) is important in many human diseases, and is regulated by a multitude of factors, including the cytokine interferon-gamma (IFNgamma). The importance of IFNgamma is highlighted in experimental autoimmune encephalomyelitis (EAE), an animal model of CNS inflammation. Mice lacking IFNgamma show exaggerated disease, with a different pattern of chemokine expression than the wild-type. We administered IFNgamma to the CNS using intrathecal injection of a replication-defective adenoviral vector to ask about direct actions of IFNgamma on chemokine expressi

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39

Forster, Thorsten. "Statistical modelling of masked gene regulatory pathway changes across microarray studies of interferon gamma activated macrophages." Thesis, University of Edinburgh, 2014. http://hdl.handle.net/1842/9558.

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Interferon gamma (IFN-γ) regulation of macrophages plays an essential role in innate immunity and pathogenicity of viral infections by directing large and small genome-wide changes in the transcriptional program of macrophages. Smaller changes at the transcriptional level are difficult to detect but can have profound biological effects, motivating the hypothesis of this thesis that responses of macrophages to immune activation by IFN-γ include small quantitative changes that are masked by noise but represent meaningful transcriptional systems in pathways against infection. To test this hypothe

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40

Bartlett, Emmalene J. "Efficacy and Immunological Mechanisms of Type I Interferon Gene Therapy in Murine Cytomegalovirus." Murdoch University, 2002. http://wwwlib.murdoch.edu.au/adt/browse/view/adt-MU20040706.134351.

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This thesis presents a comparative analysis of the type I Interferon (IFN) subtypes and an evaluation of their potential as DNA vaccines in a model of murine cytomegalovirus (MCMV) infection and disease. MCMV induces acute and chronic phases of myocarditis, a heart disease characterised by an inflammatory cell infiltrate, in susceptible BALB/c mice. The type I IFNs comprise 14 IFNá genes in the human and >10 IFNá genes in the mouse with a single IFNâ gene in both species, however, the purpose of their multiplicity has remained unclear to date. An extensive panel of murine type I IFN subtype g

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41

Bartlett, Emmalene J. "Efficacy and immunological mechanisms of type 1 interferon gene therapy in murine cytomegalovirus." Bartlett, Emmalene J. (2002) Efficacy and immunological mechanisms of type 1 interferon gene therapy in murine cytomegalovirus. PhD thesis, Murdoch University, 2002. http://researchrepository.murdoch.edu.au/214/.

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This thesis presents a comparative analysis of the type I Interferon (IFN) subtypes and an evaluation of their potential as DNA vaccines in a model of murine cytomegalovirus (MCMV) infection and disease. MCMV induces acute and chronic phases of myocarditis, a heart disease characterised by an inflammatory cell infiltrate, in susceptible BALB/c mice. The type I IFNs comprise 14 IFN alpha genes in the human and >10 IFN alpha genes in the mouse with a single IFN beta gene in both species, however, the purpose of their multiplicity has remained unclear to date. An extensive panel of murine type

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42

Kumaran, Jyothi. "The role of the SD100A domain in IFNAR1 in type I interferon signaling." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape8/PQDD_0002/MQ46202.pdf.

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43

Beauregard, Caroline. "Type I Interferon-Mediated Killing of Cancer Cells with IAP-Targeted Combination Immunotherapy." Thesis, Université d'Ottawa / University of Ottawa, 2016. http://hdl.handle.net/10393/34201.

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SMAC mimetic compounds (SMCs) are small molecule antagonists of the Inhibitor of Apoptosis (IAP) family of proteins. Binding of SMCs to the IAPs results in the sensitization of cancer cells to apoptosis in the presence of death ligands, such as tumour necrosis factor alpha (TNFα). I hypothesize that type I interferon (IFN) stimulation in cancer cells and in immune cells leads to the production of TNFα, which can then synergize with SMCs to kill cancer cells. The combined treatment of SMC and IFNα induces tumour regression in mice, and this effect is completely abrogated upon treatment with TNF

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Lee, L. N. "Characterization of type 1 interferon production during persistent lymphocytic choriomeningitis virus (LCMV) infection." Thesis, University College London (University of London), 2006. http://discovery.ucl.ac.uk/1445734/.

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Type 1 interferons (B5N-a/ps), are innate cytokines possessing important immunomodulatory and effector roles in the innate and adaptive response. They are transiently induced to very high levels during the initial stages of many viral infections. However, regulation of EFN-a/p production during persistent viral infections is not well understood. This project aimed to address these issues using the murine lymphocytic choriomeningitis virus (LCMV) infection model. Initial objectives were to develop assays that would allow characterisation of the EFN-a/p response during chronic LCMV infection in

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45

Aintablian, Haig. "Transcriptional Regulation of the Type 1 Interferon Response by a Nuclear Pore Protein." Thesis, The University of Arizona, 2018. http://hdl.handle.net/10150/627145.

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Aintablian, Haig. "Transcriptional Regulation of the Type I Interferon Response by a Nuclear Pore Protein." Thesis, The University of Arizona, 2018. http://hdl.handle.net/10150/626840.

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Salomon, Rachelle. "Regulation of Type I Interferon effects during viral infections by altering accessibility of signal transducer and activator of transcription factors /." View online version; access limited to Brown University users, 2005. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&res_dat=xri:pqdiss&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&rft_dat=xri:pqdiss:3174670.

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Fjellman, Ellen V. F. "A Protein Coding Variant in IRF7 is associated with SLE Risk and Affects Production of Type IIinterferon." University of Cincinnati / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1627662131455655.

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49

Carlsson, Lennart. "Aspects of interferon alpha signalling in hematopoetic cells." Doctoral thesis, Umeå : Univ, 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-318.

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50

Blomberg, Stina. "Autoantibodies and the Type I Interferon System in the Etiopathogenesis of Systemic Lupus Erythematosus." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3358.

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