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1
Ramshaw, Anna Louise. "Immunological aspects of human atherosclerosis." Thesis, University of Oxford, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.305549.
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Havranek, Erik Georg Ulrich. "Immunological aspects of renal cancer." Thesis, St George's, University of London, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.430426.
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Porter, S. R. "Immunological aspects of rapidly progressive periodontitis." Thesis, University of Bristol, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.377350.
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Kong, Wai-kwan Wendy, and 江慧君. "The effects of immune activation in the pathogenesis of neurodevelopmental disorders : in vivo and in vitro animal studies." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/197539.
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Schizophrenia and autism are psychiatric disorders with a presumed neurodevelopmental origin, characterised by clinical features and aetiologies that overlap at multiple levels. In addition to genetic susceptibility, epidemiological studies revealed an association between environmental factors and these disorders. Immune activation in response to infection at early gestation has been identified as one of the key risk factors. Little is known about the underlying mechanism during maternal immune activation (MIA), but extrinsic apoptotic dysregulation has been postulated to play a role in MIA infection. In particular, emerging studies suggest apoptosis without triggering whole cell demise, namely synaptic apoptosis, is a potential event that leads to the abnormal behaviours in the affected offspring.
In this study, C57BL/6N mice model was employed to investigate the impacts of viral mimetic polyriboinosinic-polyribocytidylic acid (Poly I:C) exposure at gestation day 9 in the resultant male offspring in adulthood in vivo by different parameters, including magnetic resonance imaging (MRI), behavioural tasks that assess sensorimotor gating, exploratory and anxiety behaviours, and protein quantification in the apoptotic pathway. In parallel, the direct effect of Poly (I:C) treatment for 24 hours on extrinsic apoptotic proteins were determined in primary cortical neurons in vitro. It was hypothesised that MIA would result in brain volumetric changes subsequent to behavioural anomalies in the adult offspring with maternal exposure to Poly (I:C), for which abnormalities are normally pronounced by that time. In addition, the hypothesis that foetuses exposed to Poly (I:C) in early gestation stage would have increased expression level of apoptotic proteins of extrinsic types, namely Fas receptor, caspase-8 and the death effector caspase-3.
This study found that, although male adult offspring with early maternal exposure to Poly (I:C) had an increase in raw whole brain volume, this was not significant when body weight was included as a covariable. However, prenatal exposure caused behavioural features similar to those reported in schizophrenia and autism such as prepulse inhibition deficits, increased anxiety-level and higher locomotor activity in response to amphetamine challenge. On the other hand, a marked augmentation in caspase-8 level without any significant changes in Fas or caspase-3 was observed in the adult hippocampus. No alterations in the expression of selected apoptotic proteins were found in the embryonic cortical cells.
Overall the present studies suggested that acute exposure to infection during early fetal development causes a range of aberrations in brain anatomy, behaviour and biochemistry that are of relevance to the pathophysiology of schizophrenia and autism. The results suggest a potential involvement of synaptic apoptosis in cellular events underlying neurodevelopmental disorders.published_or_final_version
Psychiatry
Master
Master of Philosophy
5
Neumann, Andersen Grethe. "Systemic sclerosis : vascular, pulmonary and immunological aspects." Doctoral thesis, Umeå universitet, Reumatologi, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1806.
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In systemic sclerosis (SSc), interstitial lung disease (ILD) and engagement of the vascular system lead to increased morbidity and mortality. The aim of this thesis was to elucidate, in a consecutively included cohort of SSc (limited and diffuse) patients (n = 33), the T cell cytokine profile driving the disease in ILD and to explore the role of matrix metalloproteinase 9 (MMP-9) and its inhibitor: tissue inhibitor of metalloproteinase 1 (TIMP-1) in the extracellular matrix (ECM) degrading process leading to fibrous scarring and honey combing. Moreover, to characterize the role of nitric oxide (NO) in vascular engagement. Peripheral arterial changes cause Raynaud’s phenomenon and digital ulcers. Nitric oxide (NO) a main inducer of vasodilation is produced by endothelial nitric oxide synthase (eNOS) in response to changes in blood flow or by inflammatory cytokine inducible (i) NOS. In the vascular smooth muscle cell (VSMC) NO activates guanylate cyclase to produce cGMP, causing relaxation. We showed elevated plasma nitrate, a degradation product of NO, and increased urinary excretion of nitrate and cGMP. Plasma nitrate correlated with elevated levels of endothelial adhesion molecules: endothelial (E) selectin and vascular adhesion molecule 1, indicating that the activated endothelium is the site of NO synthesis by iNOS. Endothelial staining for E-selectin and the finding of iNOS and eNOS in SSc skin biopsies supported this notion. In SSc increased vascular stiffness may limit the NO vasodilatory effects. We found normal endothelium-dependent (i.e. flow mediated (FMD%)) and endothelium-independent (i.e. nitroglycerin-induced (NTG%)) vasodilation in the brachial artery. Radial arterial wall stiffness measured as maximum increase in pulse pressure (dP/dtmax) was increased. FMD% and especially NTG% correlated negatively and dP/dtmax positively to measures of endothelial inflammation: plasma- nitrate and adhesion molecule levels. Thus inflammatory vascular wall changes may interfere with dilation as may the presence of nitrate tolerance. We found elevated alveolar MMP-9 in both its pro- and active form in ILD. The levels correlated to decline in lung capacity, pointing at a causal relation. We suggest that neutrophils secrete MMP-9, which may degrade collagen IV, (the main constituent of basal membranes), collagen V, gelatins, proteoglycans and elastin. MMP-9 activity is partly regulated by the binding of pro- and active form to TIMP-1. Alveolar TIMP-1, which even stimulates fibroblast ECM synthesis, was increased independent of ILD. The inflammatory process in ILD is orchestrated by activated T helper (h) lymphocytes. We found a mixed Th1/Th2 reaction in SSc alveolar T cells expressing messenger for interferon gamma (Th1), IL-6 and IL-10 (both Th2). No particular cytokine mRNA profile distinguished alveolar T cells in ILD. Neutrophils invaded the bronchial epithelium, which seemed otherwise inert as levels of inflammatory cytokine sensitive transcription factors and their nuclear translocation tended to be low. The neutrophil recruitment pathway is uncertain as chemoattractants and endothelial adhesion molecules were normally expressed. In conclusion, MMP-9 probably causes degradation of lung tissue in ILD and may represent a future therapeutic target. Alveolar T cells show a mixed Th1/Th2 cytokine profile independent of ILD. Neutrophils invade the bronchial epithelium. Activated endothelium produces increased amounts of NO and adhesion molecules and the level of activation influences brachial arterial FMD% and NTG% and radial arterial compliance. Nitrate tolerance may be present.
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Sjöwall, Johanna. "Clinical and Immunological Aspects of Lyme borreliosis." Doctoral thesis, Linköpings universitet, Infektionsmedicin, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-68745.
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Lyme borreliosis (LB) is a tick-borne infection caused by spirochetes of the Borrelia (B.) burgdorferi sensu lato complex. The infection is associated with several clinical features, of which erythema migrans (EM) and neuroborreliosis (NB) are the most common in Europe. The prognosis after antibiotic therapy is generally good. However, some patients may have residual symptoms post-treatment. The cause of the delayed convalescence is unclear. There are several factors that may affect the clinical outcome of LB, for example, the early interaction between the host’s immune response and B. burgdorferi, the spirochete genotype, antibiotic therapy, as well as the host’s vulnerability. This thesis aimed to explore the type of early immune response that is generated to B. burgdorferi and its importance for the clinical outcome of LB, and to study the condition of persistent symptoms post-NB from clinical, immunological and diagnostic perspectives. In total, 125 adult patients with different clinical features and outcomes of LB and 23 healthy controls were included. In a prospective follow-up study of EM, we confirmed that the prognosis of EM is good after antibiotic therapy, and that B. afzelii is the most common B. burgdorferi genotype associated with EM in the Nordic countries. Seven patients (8%) reported persistent symptoms more than six months post-treatment. These patients had also a decreased early expression of inflammatory, Th1-type cytokines in the EM lesions, suggesting an importance of early, local Th1-type immunity to B. burgdorferi for a successful clinical outcome of LB. No correlation between clinical characteristics, allergic predisposition, B. burgdorferi genotype or serology and the development of symptoms post-treatment was found. Asymptomatic B. burgdorferi-seropositive individuals are interesting from clinical and immunological points of view, since they apparently have encountered B. burgdorferi without developing symptoms of LB. In this thesis, asymptomatic individuals were shown to display an enhanced innate inflammatory immune response to live B. garinii spirochetes, induced by dendritic cells and whole blood cells, in comparison with patients with a history of subacute NB and healthy controls. Whether this is the optimal immune response to B. burgdorferi remains to be determined. A randomized, placebo-controlled cross-over study showed that three weeks of doxycycline therapy did not significantly improve objective neurological signs, subjective symptoms or quality of life in NB patients with persistent symptoms post-treatment. Nor could any doxycycline-mediated effects on systemic cytokine responses be demonstrated. Brain magnetic resonance imaging (MRI) findings in NB patients with persistent symptoms post-treatment were shown to be nonspecific and to correlate with age, but not with the duration of symptoms. In conclusion, this thesis shows that there is an association between the early immune response to B. burgdorferi sensu lato and the clinical outcome of LB. The cause of prolonged convalescence post-treatment remains unknown and needs further investigation. However, repeated treatment with doxycycline does not lead to improvement of the persistent symptoms; nor does brain MRI facilitate diagnosis of, or provide an explanation for the post-treatment symptoms.
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Wood, Matthew John Andrew. "Immunological aspects of neural transplantation in rodents." Thesis, University of Oxford, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.333298.
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Calvet, Christophe. "Immunological aspects of anticancer electroporation-based treatments." Thesis, Paris 11, 2014. http://www.theses.fr/2014PA114816.
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L'électrochimiothérapie est un traitement anticancéreux utilisé en routine en Europe dans près de 130 centres de traitement du cancer. Le taux de réponse objective atteint 85 % pour le traitment de tumeurs cutanées et sous-cutanées et des études sont en cours afin d'appliquer ce traitement à des tumeurs profondes. Au cours de ce doctorat, les méchanismes sous-jacents à cette excellente efficacité antitumorale ont été étudiés. Dans un premier temps, l'objectif a été d'évaluer la capacité de l'électrochimiothérapie à induire la mort des cellules souches cancéreuses, considérées comme les racines du cancer. Ensuite, les mécanismes immunologiques à l'origine du développement d'une immunité antitumorale mise en place par le traitement ont été investigués. Cependant, malgré le haut taux de réponse observé, l'électrochimiothérapie reste un traitement local qui n'induit pas de réponse antitumorale à distance, sur les tumeurs non-traitées. Afin de pallier à cette absence d'activité systémique, une collaboration a été mise en place avec une entreprise innovante de biotechnologies, INVECTYS, dans le but de développer une stratégie de vaccination à ADN ciblant la télomérase et basée sur l'électrogènetransfert. Il est attendu que la combinaison de cette immunothérapie avec un traitement local par électrochimiothérapie, détruise non seulement la tumeur primaire, dont les cellules souches cancéreuses, mais également les cellules cancéreuses circulantes et les métastasesElectrochemotherapy is an anticancer treatment used in routine in Europe in 130 cancer treatment centers. The objective response rate reaches 85 % for the treatment of cutaneous and subcutaneous tumors and studies are ongoing to spread the use of electrochemotherapy to deep-seated tumors. In the frame of this doctorate, the mechanisms underlying this excellent antitumor efficiency were investigated. First, the goal was to evaluate the ability of electrochemotherapy to induce the death of cancer stem cells, considered as the roots of cancer. Second, the immunological mechanisms responsible for the development of antitumor immune responses following the treatment were investigated. However, although a very high response rate is observed, electrochemotherapy remains a local treatment which does not induce antitumor responses in distant non-treated nodules. In order to circumvent this lack of systemic activity, a collaborative project was initiated with an innovating biotech company, INVECTYS, in order to develop a DNA vaccination strategy targeting the telomerase and based on electrogenetransfer. It is expected that the combination of this immunotherapy with a local treatment by electrochemotherapy could destroy not only the primary tumor, including cancer stem cells, but also circulating cancer cells and metastases
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Makarenko, O., O. Molozhava, Тетяна Василівна Івахнюк, Татьяна Васильевна Ивахнюк, Tetiana Vasylivna Ivakhniuk, I. Wolfe, and R. Broz. "Microbiological and immunological aspects of Alzheimer's disease." Thesis, OMICS International Pvt Ltd, 2017. https://essuir.sumdu.edu.ua/handle/123456789/81108.
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В роботі описані результати мікробіологічних та імунологічних показників пацієнтів з хворобою Альцгеймера.В работе описаны результаты микробиологических и иммунологических показателей пациентов с болезнью Альцгеймера.
The paper describes the results of microbiological and immunological parameters of patients with Alzheimer's disease.
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Franks, Susan F. (Susan Faye). "Negative Psychological States: Predictors for Immunological Health." Thesis, University of North Texas, 1992. https://digital.library.unt.edu/ark:/67531/metadc332521/.
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Relationships of negative psychological conditions with general status of cell-mediated and humoral immune systems were investigated. A unique approach was utilized in that indexes representing multiple aspects of each branch of the immune system were employed to better indicate general immunological status. Differences in emotion-immune interactions between males and females were demonstrated. Results indicated a positive relationship between Trait Anger and Cell-Mediated Immunological Index. Particular criticisms of previous psychoneuroimmunological research were met by addressing sex differences and differences in various conditions of anger and depression, as well as through assessment of cumulative effects of negative emotions on immune system status. Directions for future research in eddressing similar issues are suggested. In general, results provide support for validity of mindbody interactionism and imply the need for revision of standard medical and psychological treatment.
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吳越 and Yuet Wu. "The study of immune response to co-infection of influenza virus and Streptococcus pneumoniae." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/193417.
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Influenza is a leading cause of respiratory disease worldwide. During pandemic and seasonal influenza, secondary Streptococcus pneumoniae infection is a severe complication that contributes to morbidity and mortality. With the clinical significance of this co-infection, it is imperative to understand the disease mechanisms and how our immune system would be modulated in dealing with the dual infection.
First, in vivo co-infection model was established. Mice were sequentially infected with influenza virus and then Streptococcus pneumoniae. Co-infected mice lost their body weight significantly and had 100% mortality, whereas mice infected with either influenza virus or pneumococcus alone lost their body weight transiently and all recovered from the infection.
Then, lung inflammatory response during the co-infection was examined. Although it is a common phenomenon that co-infection enhances inflammation, the kinetic of, and the relative contribution of influenza virus or pneumococcus to the lung inflammation is not well defined. Therefore, this study characterized the general lung inflammatory environment after co-infection. It was found that influenza virus and pneumococcus differentially modulated inflammatory response in terms of kinetics, leukocyte infiltration and cytokine production. At the early time point after co-infection, pneumococcal infection contributed more than the influenza virus infection to enhance inflammatory cytokine and neutrophil infiltrating the lung. At the later time point after co-infection, both influenza virus and pneumococcus contributed to synergistically increase inflammatory cytokine and macrophage infiltrating the lung. Influenza virus infection induced IFN-γ that contributed to the elevated IFN-γ level in co-infected mice. Influenza virus and pneumococcus synergistically increased Th2 associated cytokine including IL-4, IL-5, and IL-10. These up-regulated immune responses might contribute to the severe lung pathology.
Next, adaptive immunity to co-infection was examined. Literature studying co-infection often reports how prior influenza virus infection impairs the immune response against subsequent bacterial infection. However, whether and how secondary pneumococcal infection would affect the immunity to the initial influenza virus is unknown. Therefore this study investigated the modulation of immunity to influenza virus by secondary pneumococcal infection. It was found that co-infection significantly enhanced virus titer in lung and depleted the number of cell in spleen. Secondary pneumococcal infection after influenza decreased influenza virus specific IgG in the lung and peripheral blood. The reduced level of virus specific IgG was associated with the decrease in the number and the percentage of follicular B cell and CD4 T follicular helper cell through both pneumococcal capsular polysaccharide dependent and independent manner. Treating co-infected mice with immune serum containing influenza virus specific IgG successfully improved survival, which suggested the important protective function of virus specific IgG to the co-infection. Taken together, these data suggested that secondary pneumococcal infection impairs the antibody response to influenza virus, which might enhance mortality after co-infection.
In conclusion, this study provides new insight to understand the pathogenesis of co-infection, reveals the general lung inflammatory environment, highlights the negative role of pneumococcus to impair virus control and explores novel treatment for the co-infection.published_or_final_version
Paediatrics and Adolescent Medicine
Doctoral
Doctor of Philosophy
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Arvola, Marie. "Immunological aspects of maternal-foetal interactions in mice." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2001. http://publications.uu.se/theses/91-554-4947-6/.
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Boczkowska, Beata. "Aspects of porcine immunological response to Nipah virus." PLoS One, 2012. http://hdl.handle.net/1993/30139.
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Nipah virus (NiV) is a highly pathogenic and zoonotic paramyxovirus in the subfamily Paramyxovirinae, genus Henipavirus. The virus causes outbreaks of severe febrile encephalitis with a high mortality rate in humans, and of encephalitic and respiratory disease but with a low mortality rate in pigs.
The innate immune response has a critical role in limiting viral infection by activating antiviral state and adaptive immune response. As pigs are able to overcome the infection with NiV, the working hypothesis was that IFN induced signaling pathways are not completely inhibited by NiV in infected porcine cells enabling an antiviral state to be established. Indeed, there was no block of eIF2α phosphorylation in porcine fibroblast (ST) and monocytic-like (IPAM) cells, and human fibroblast (MRC5) cells. To address the potential activation of an alternative IFN induced pathway, the MAPK signaling pathways were examined. The findings revealed that NiV infection triggers different kinetics of phosphorylation of ERK and p38 MAPK in the selected cell types. The data also indicates that p38 MAPK to be indispensable for NiV replication in vitro especially in immune cells.
As the involvement of immune cells in viral spread and in immune modulation of porcine adaptive immune response were reported. The next hypothesis stated that NiV infects immune cells and affects the population frequencies of PBMC in pigs. In vitro, productive viral replication was detected in monocytes, CD6+CD8+ T lymphocytes and NK cells, by recovery of infectious virus, anti-genomic RNA and detection of structural N and non-structural C proteins. B lymphocytes, CD4-CD8-, as well as CD4+CD8- T lymphocytes were not permissive to NiV. In NiV infected piglets, the expansion of the CD4+CD8- T cells early post infection was consistent with a functional humoral response. In contrast, significant drop in CD4+CD8- T cell frequency was observed in piglets which succumbed to the experimental infection, supporting vaccine studies that antibody development is a critical component of protective immune response. Thus, both aspects of innate and adaptive immune response are affected and contribute to NiV pathogenesis. These findings will help researchers to design and establish vaccination programs that would be more effective in pigs.
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Hedin, Skogman Barbro. "Neuroborreliosis in childhood : Clinical, immunological and diagnostic aspects." Doctoral thesis, Linköpings universitet, Pediatrik, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-11520.
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Lyme Borreliosisis is a multi-organ infectious disease caused by the spirochete Borrelia burgdorferi. The spirochete is transmitted to humans by tick bites. Neuroborreliosis (NB) is a disseminated form of the disease, in which the spirochetes invade the nervous system. In children, subacute meningitis and facial nerve palsy are typical clinical manifestations of NB. The aim of this thesis was to study clinical, immunological and laboratory characteristics in children being evaluated for NB in a Lyme endemic area of Sweden, in order to identify factors of importance for prognosis and clinical recovery. A total of 250 patients and 220 controls were included during 1998-2005, with a prospective and a retrospective part. Less than half (41%) of children with signs and symptoms indicative of NB get the diagnosis confirmed by detection of Borrelia specific flagella antibodies in CSF (clinical routine method). Surprisingly few patients were diagnosed as having other infectious or neurologic diseases and consequently, many patients ended up with an uncertain diagnosis. However, four new Borrelia antigens (DbpA, BBK32, OspC, IR6) were evaluated and performed well in laboratory diagnostics. If they were combined in a panel, together with the flagella antigen, the sensitivity was 82% and the specificity 100%, leading to improved diagnostic accuracy in children with NB, as compared to using the routine flagella antibody test alone. Clinical recovery at the 6-month follow-up (n=177) was generally good and nonspecific symptoms, such as headache and fatigue, were not more frequently reported in patients than in controls. No patient was found to have recurrent or progressive neurologic symptoms. However, permanent facial nerve palsy was found in 22% of patients at the 2-year follow-up, with consequences such as eye-closing problems, excessive tear secretion, pronunciation difficulties and cosmetic complaints. When cellular immune responses were investigated, the number of Borrelia-specific IL-4 and IFN-γ secreting cells in CSF was found to be more prominent in children with NB than in controls. Furthermore, a much stronger IL-4 response in CSF was seen in children as compared to adults with NB. This cytokine profile of children with NB is believed to represent an effective and balanced type1/type2 response in a relevant compartment, and could contribute to the less severe course of the disease seen in children as compared to adults with NB. No prognostic factors were found to influence the outcome in patients with “Confirmed NB” or facial nerve palsy. Nor was any specific cytokine profile, or antibody response to new Borrelia antigens in CSF, correlated to a less favorable clinical outcome. An NB prediction score test, based on clinical variables at admission, is suggested to help physicians to determine whether to start early antibiotic treatment, before results from Borrelia antibody tests are available. Results in this thesis support the notion that mononuclear pleocytosis in CSF, in patients being evaluated for NB, indicates that they are true NB cases despite the fact that an antibody response cannot yet be visualized. with the routine flagella test. Consequently, early antibiotic treatment in NB seems to be the correct course of action and over-treatment is not a substantial problem.Borrelia-infektion hos barn och vuxna är den vanligaste fästingburna infektionen i Sverige och orsakas av en bakterie som heter Borrelia burgdorferi. Den sprids till människa via fästingbett och kan orsaka besvär från hud, leder, hjärtmuskel och nervsystem. När nervsystemet är infekterat kallas det Neuroborrelios. Denna avhandling handlar om Neuroborrelios hos barn i syd-östra Sverige, ett område med hög Borrelia-förekomst. Jag har studerat symtom, laborativa provsvar och tillfrisknande hos 250 barn med misstänkt Neuroborrelios under åren 1998-2005 och jämfört med friska barn. Dessutom har jag tittat närmare på vissa signalsubstanser inom immunförsvaret i blod och ryggvätska och vilken roll signalsubstanserna spelar för förlopp och utläkning av infektionen. Avhandlingen innehåller också en utvärdering av fyra nya diagnostiska test vid misstänkt Neuroborrelios hos barn. Det visar sig att mindre än hälften (41%) av barnen med misstänkt Neuroborrelios får diagnosen säkerställd med det befintliga Borrelia-testet (baserat på ett protein som kallas flagellin) som används rutinmässigt. Dock förblir diagnosen oklar för många barn (59%). De fyra nya Borrelia-testen (baserade på protein som kallas DbpA, BBK32, OspC och IR6) visar sig fungera bra och om man kombinerar dem med befintligt Borrelia-test, kan man säkerställa Neuroborrelios hos 82% av barnen med misstänkt infektion. Jag hoppas att dessa nya Borrelia-test i framtiden kan leda till förbättrad diagnostik hos barn som utreds för misstänkt Neuroborrelios. Immunförsvarets signalsubstanser, som analyserades i ryggvätska och blod, visade sig ha en viss profil hos barn med Neuroborrelios jämfört med barn utan Borrelia-infektion, men även jämfört med vuxna med Neuroborrelios. De immunologiska T cellerna producerade två olika sorters signalsubstanser, som kallas ”Interferon-γ” och ”Interleukin-4”. Denna immunologiska profil verkar fördelaktig och kan möjligen bidra till den i allmänhet goda utläkning av Neuroborrelios som man ser hos barn jämfört med vuxna. De vanligaste symtomen vid en Borrelia-infektion i nervsystemet är huvudvärk, trötthet, dålig aptit, feber och ont i nacken. Ansiktsförlamning är det vanligaste specifika neurologiska symtomet. Antibiotikabehandling ges till 69% av barnen och vid en 6 månaders uppföljning rapporterar patienterna god utläkning av de olika symtomen. Inget barn hade återkommande eller allvarliga neurologiska symtom vid uppföljningen. Däremot, barn med ansiktsförlamning visade sig få kvarstående besvär i viss utsträckning. När de undersöktes 2 år efter sin ansiktsförlamning förekom mild till måttlig kvarstående förlamning i 22% av fallen. Patienterna uppgav besvär av ökat tårflöde, sluddrigt tal, svårigheter med att stänga ögat och dessutom rapporterade många patienter att snedheten i ansiktet var kosmetiskt störande. Inga specifika symtom, laborativa prov, immunologiska signalsubstanser eller diagnostiska test visade sig vara kopplade till ökad risk för kvarstående besvär efter Neuroborrelios i allmänhet och inte eller hos patienter med ansiktsförlamning. En checklista har utarbetats med olika symtom som är typiska för barn med Neuroborrelios. Den föreslås kunna användas som beslutsunderlag för start av tidig antibiotikabehandling, redan innan svar på Borrelia-testen finns tillgängliga.
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Kennedy, Rebekah Storm. "Microbiological and immunological aspects of equine periodontal disease." Thesis, University of Glasgow, 2017. http://theses.gla.ac.uk/8064/.
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Periodontal disease is a common and painful condition in the horse. Although awareness of the condition is growing amongst the veterinary profession and horse owners, the presence of the disease is often overlooked and treatment can be difficult. Despite this, there have been few recent studies of the aetiopathogenesis of the condition. Certain species of bacteria may act as periodontal pathogens, stimulating a destructive inflammatory response in periodontal tissues and this has been well recognised as being important to the aetiopathogenesis of the disease in man. However few equine studies on this aspect of the disease have been carried out. The main aims of this study were: - 1) to identify the bacteria associated with a healthy oral cavity and periodontitis in horses using culture dependent and independent methods; 2) to assess the differences in bacterial populations between the healthy and periodontitis groups and identify putative pathogens; 3) to quantify the expression patterns of TLRs 2, 4 and 9, the pro-inflammatory cytokines IL-1β and TNFα, anti-inflammatory cytokine IL-10 and Th1/Th2/Th17 cytokines IL-4, IL-6/ IL-12, IFNɣ/ IL-17, within gingival tissue from each sample group; 4) to use matched data to establish if associations exist between the presence and quantity of bacterial species present and TLR expression and 5) to determine activation of TLRs 2, 4 and 9 by putative pathogens using specific in- vitro TLR assays. Swabs were taken from the gingival sulcus of 42 orally healthy horses and plaque samples were taken from the periodontal pockets of 61 horses with periodontal disease. The location and grade of the lesion was noted and an equine dental chart completed for each case. Bacteria were identified using high throughput 16S rRNA gene sequencing, QPCR, whole genome sequencing and conventional culture followed by 16S gene sequencing. Gingival biopsies were taken from 13 orally healthy horses and 20 horses with periodontitis and gene expression of TLR 2, TLR 4, TLR 9, IL-1β, IL-4, IL-6, IL-10, IL-12, IL-17, TNFα and IFNɣ was measured. THP-1X Blue, MyD88 THP-1X Blue, HEK hTLR 2 Blue and HEK hTLR 4 Blue human cell lines were co-cultured with putative periodontal pathogens and their response measured via level of secreted embryonic alkaline phosphatase. Clinical, microbiological and immunological data underwent cross-matching analysis. Microbial populations showed 89% dissimilarly between oral health and periodontitis with a less diverse population present in diseased equine periodontal pockets. The most discriminative bacteria between health and disease identified at genus level were Fusobacteria and Acinetobacter in health and Pseudomonas and Prevotella in periodontitis. The most abundant genera were Gemella (36.5%), Pseudomonas (14%) and Acinetobacter (8%) in orally healthy samples and Pseudomonas (25%), Prevotella (14%) and Acinetobacter (9.4%) in periodontitis samples. Whole genome sequencing revealed the presence of 75 species of Prevotella in the equine oral cavity and a significantly higher number of reads corresponding to Prevotella bivia, Prevotella dentalis, Prevotella denticola, Prevotella intermedia, Prevotella melaninogenica, Prevotella nigrescens were noted in diseased samples. Significant increases in expression of TLR 4 mRNA, TLR 9 mRNA and, in particular TLR 2, mRNA were noted in diseased equine gingival tissue in addition to increased pro-inflammatory and anti-inflammatory cytokine mRNA expression. Presence of P. intermedia was significantly positively correlated with expression of TLR 2 in equine periodontitis. In addition, the presence of Aggregatibacter actinomycetemcomitans was positively associated with disease severity and expression of TLR 4 mRNA in the horse. Co-culture of periodontal pathogens with human cell lines revealed that the innate immune response to the presence of these bacteria is mainly mediated through TLR 2 activation. The use of both culture dependent and culture independent methods to investigate the equine oral microbiome has provided significant breadth and depth of information on the microbiology of equine periodontal disease. Microbial populations are significantly different as expected and bacteria belonging to the Prevotella genus have been strongly implicated in the aetiopathogenesis of the condition. The innate immune response produced in periodontally diseased equine gingival tissue has been characterised for the first time in the horse.
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何柏松 and Pak-chung Ho. "Immunological studies in gestational trophoblastic disease." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1989. http://hub.hku.hk/bib/B31981343.
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Middlemiss, Melanie Jane, and n/a. "Aspects of a computational model inspired by immunological principles." University of Otago. Department of Information Science, 2007. http://adt.otago.ac.nz./public/adt-NZDU20071220.150157.
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Nature and biological systems have provided the basis for many computational models and systems, such as neural computing and evolutionary computation. This thesis examines the vertebrate immune system which formed the original basis for Artificial Immune Systems (AIS). The vertebrate immune system is highly complex and, for the most part, is successful at providing us with protection from harmful stimuli. Such a system is attractive as a model to inspire a computational system as it exhibits many desirable behaviours: adaptability, diversity, robustness, efficiency and multiple layers of detection.
There has been an increasing volume of research in the field of artificial immune systems. However, as the field has expanded, immunological analogies have been reduced at the expense of problem specific optimisation. Hence, this thesis takes a different approach and returns to the immune system which initially inspired research in this field.
In this thesis a set of key immunological properties based on immune system concepts and mechanisms are formalised in a model for an artificial immune system. This leads to an AIS framework that is more closely aligned with the immune system, and incorporates both innate and adaptive immune concepts. In particular, antigen presenting cells (APCs), major histocompatibility complex (MHC) molecules and T-cells are modelled within the framework. The differential signalling hypothesis is explored as a model for T-cell development, and provides a novel method for T-cell generation within an AIS.
Extensive empirical analysis is performed at an individual level to examine the behaviour of the AIS framework components. These results show that the artificial immune system components exhibit similar properties to the real immune components that inspired them. However, the MHC component of the AIS is found to be of limited value within an individual AIS. The AIS framework is subsequently extended to model a population of artificial immune systems. Further empirical analysis is performed at a population level, and MHC is found to improve the adaptability of an evolving population of artificial immune systems within a dynamic environment.
Such a model of immune system function is likely to be useful for immunologists, as it could provide a method of examining immune behaviour under various conditions in a cheaper and more rapid manner than in-vivo or in-vitro. Indeed, it may also provide a solution for examining properties that are unable to be tested using these traditional methods. Finally, the results of these empirical findings are discussed in terms of the relevance and applicability of immunological principles with regard to artificial immune systems for real world problems.
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Norbeck, Oscar. "Clinical and immunological aspects of human parvovirus B19 infection /." Stockholm : Dept. of laboratory medicine, Karolinska institutet, 2005. http://diss.kib.ki.se/2005/91-7140-203-9/.
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Wu, Yuet, and 吳越. "Immune response of human monocyte-derived dendritic cells to co-infection of influenza virus and Streptococcus pneumoniae." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B45543732.
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Li, Jian, and 李健. "Interleukin 17A and interleukin 23 in chronic hepatitis B and hepatocellular carcinoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B45875790.
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Effertz, Bernard Stephen. "The humoral immune response to streptococcal cell wall-induced arthritis in the rat." Diss., The University of Arizona, 1989. http://hdl.handle.net/10150/184877.
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I investigated the humoral immune response to streptococcal cell walls (SCW) in arthritis susceptible Lewis and resistant Fisher rats. All rats were given a single intraperitoneal injection of either SCW or saline (controls). Rats were sacrificed, three rats per time point, over an eleven week period and serum was collected for ELISA. SCW injected Lewis rats produced anti-SCW antibody, whereas control rats did not. Anti-SCW antibody was significantly elevated over controls between days 14-28 (post injection). Both saline and SCW injected Fisher rats produced anti-SCW antibody, but with different kinetics. Anti-SCW antibody increased by day 7 and remained elevated over controls till day 21, after which there was no difference. ELISA were designed to determine the SCW epitope(s) recognized by anti-SCW antibody. Formamide extracts of SCW, peptidoglycan and polysaccharide, were investigated along with the terminal epitope of polysaccharide, N-acetyl-D-glucosamine, and the peptidoglycan precursor peptide. The data revealed that anti-SCW antibody was directed against a combined SCW epitope, given the lack of significant binding to any of the SCW epitopes tested. Isotype analysis of anti-SCW antibody revealed that the Lewis response was composed primarily of IgG2a whereas the Fisher response was composed primarily of IgM. Binding of rat IgG isotypes to whole streptococcus, SCW, peptidoglycan, and polysaccharide was investigated, given the possibility of background binding by the streptococcal Fc-receptor. Streptococcal binding of rat IgG was specific for IgG2c and the polysaccharide portion of SCW was necessary for binding. Passive immunization of naive Lewis rats with antibody from rats with active arthritis was ineffective at transferring the disease. However, subcutaneous injection of affinity purified anti-SCW antibody or IgG into Lewis rats, followed twenty-four hours later by a single intraperitoneal injection of SCW, suppressed the acute phase and inhibited the chronic disease. IgM rheumatoid factor (RF) was present in the serum of both saline and SCW injected Lewis and Fisher rats. However, SCW injection only induced a significant increase in IgM RF (between days 3-7) in Lewis rats. Passive immunization of Fisher rats with affinity purified IgM RF (from Lewis serum), three days post SCW injection, was ineffective at inducing arthritis.
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Linher, Katja. "Association of markers in genes of the growth hormone axis with the viral load in lymphoid tissues of chickens infected with Marek's disease virus." Thesis, McGill University, 2000. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=33420.
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Vaccination against Marek's disease (MD) is greatly enhanced by host genetic resistance. Genes of the growth hormone (GH) axis have been reported to affect the ontogeny and effector functions of cells of the immune system. Two strains of White Leghorn chickens bred for contrasting homozygous markers in the GH and GH receptor (GHR) genes were challenged with MDV. Contrasts for the significant interaction between marker genotype and tissue indicated that the GH/GHR marker genotype caused a shift in the distribution of the viral load in lymphoid tissues in the two strains. The analysis suggests that genetic variations in genes of the GH axis may differentially affect the host response to MDV replication in lymphoid tissues. Regarding the early time course of infection, at day 6 the viral load was highest in the thymus, while at day 10, it was highest in the spleen, indicating that the virus may have accumulated in the spleen or was continuing to replicate in this tissue. (Abstract shortened by UMI.)
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Masilamani, Twinkle Jasmine. "Identification of genetic markers associated with Marek's disease resistance in chickens." Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=19691.
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Marek's disease (MD) is a highly contagious and economically important disease in the poultry industry. It is caused by an oncogenic avian herpes virus. The ability of the virus to evolve into new strains is a continual threat. Vaccination, proper management and genetic resistance are required to completely eliminate the pathogen. The discovery of several markers associated with MD resistance shows that genetic selection for resistance is feasible. Our objective was to identify markers in QTL regions that are associated with MD viraemia. The markers analysed were in the ODC gene, the GH gene and two chemokine genes, all of which are candidate genes for immune responsiveness. A database in a commercial strain of White Leghorn chickens was created. Heterozygous males and homozygous females were identified. The offspring were challenged with MD virus and spleen and thymus samples were collected six days after infection. The viral titre was quantified using competitive PCR. The data was analysed using non-parametric statistics. We found that the paternal alleles of a Hindlll RFLP in the ODC gene were associated with differences in MD viraemia in one of the six sire families analysed. In addition, a Sacl RFLP located in the GH gene also segregated for alleles, which affected MD viraemia. The analysis of the ODC gene was extended to include a second RFLP at a Msp\ site. Together with the Hindlll RFLP it defines three different haplotypes. One genotypic class AB (Hindlll (+/-), Mspl (+/+)) was associated with low vireamia in the thymus and the genotype BB (Hindlll (-/-), Mspl (+/+)) with high viraemia in the spleen. The result suggests that genetic variations in the ODC and GH gene affect MD viraemia. However, we cannot exclude that the observed effects might be due to linkage disequilibrium with adjacent genes. In the latter case, chromosome 3 and chromosome 1, which harbour the ODC and GH gene respectively, must segregate for regions that affect viraemia. The markers identified in this analysis can be used in marker assisted selection.
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Ahvazi, Behrouz C. "Mechanisms of modulation of immune responses during blood-stage malaria." Thesis, McGill University, 1994. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=26454.
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In this thesis, mechanisms of immunoregulation by CD4$ sp+$ T cells during blood-stage P. chabaudi AS infection in C57BL/6 mice were studied. The kinetics of in vitro production of the Th1-derived cytokine, IFN-$ gamma$, versus the Th2-derived cyokines, IL-4, IL-5 and IL-10, by spleen cells as well as of polyclonal and malaria-specific antibodies in the sera were examined during infection using enzyme-linked immunosorbent assays. Upon antigenic stimulation, spleen cells were found to produce high levels of IFN-$ gamma$ several days prior to peak parasitemia, while high levels of IL-10 production occurred at the time of peak parasitemia followed by IL-4 and IL-5 later in infection. The levels of polyclonal IgG2a isotype were found to be increased during both the acute and chronic phases of infection, whereas the levels of polyclonal IgM, IgG1 and IgG2b isotypes were found to be increased only during the chronic phase of infection. High titers of malaria-specific IgG2a and IgG1 were detected during the primary as well as secondary infections. Investigation of in vitro proliferation of spleen cells to mitogens and malaria specific antigen revealed that the responses of splenic lymphocytes from infected mice to Con A, PHA and LPS were suppressed, with the most severe suppression occurring during the first 14 days post infection. Evidence is provided demonstrating that nitric oxide (NO) and prostaglandins (PG), products of activated macrophages, mediated suppression of lymphocyte proliferation in response to Con A and PHA, whereas only PG were found to suppress LPS-stimulated proliferation. In addition, NO was found to mediate suppression of proliferation of spleen cells from infected mice in response to parasite antigen. Taken together, results from these studies suggest that immune activation and immunosuppression occur simultaneously during blood-stage malaria with P. chabaudi AS infection in C57BL/6 mice. (Abstract shortened by UMI.)
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de, Boniface Jana. "Sentinel Node Biopsy in Breast Cancer : Clinical and Immunological Aspects." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-7890.
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Pidverbetska, O. V., D. V. Kovtun, and M. І. Ostafiychuk. "Immunological aspects of immune reconstitution inflammatory syndrome in HIV-infection." Thesis, БДМУ, 2021. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/18025.
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Hjorth, Maria. "Immunological profile and aspects of immunotherapy in type 1 diabetes." Doctoral thesis, Linköping : Department of Clinical and Experimental Medicine, Linköping University, 2010. http://www2.bibl.liu.se/liupubl/disp/disp2010/med1161s.pdf.
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Walton, Shelley Faye. "Sarcoptes scabiei : a molecular approach to immunological and epidemiological aspects." Thesis, The University of Sydney, 1999. https://hdl.handle.net/2123/27676.
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The aim of this project was to account for and characterise the extent of genetic variation within and between sympatfic host-associated populations of dog-derived and human-derived Sarcoptes scabiei.
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Hartaningsih, Nining. "Aetiological and immunological aspects of Jembrana disease in Bali cattle." Thesis, Hartaningsih, Nining (1993) Aetiological and immunological aspects of Jembrana disease in Bali cattle. PhD thesis, Murdoch University, 1993. https://researchrepository.murdoch.edu.au/id/eprint/53267/.
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The clinico-pathological changes in experimentally induced Jembrana disease in Bali cattle (Bos javanicus) were determined as a basis for the differential diagnosis of the disease and increased understanding of the pathogenesis of the disease process. The incubation period varied from 4 to 12 days. The major clinical signs in the experimentally infected cattle were an elevated rectal body temperature persisting for 5 to 12 days, lethargy, anorexia, and enlargement of the superficial lymph nodes. The case fatality rate was 17%. The major haematological changes included a leukopenia characterized by a lymphopenia, eosinopenia and slight neutropenia. There was also a mild thrombocytopenia, anaemia, elevated blood urea levels (especially marked in those animals that died) and a reduced total plasma protein level. The clinical and haematological changes were most marked during the febrile period.
Crossbred Bali (Bos javanicus x Bos indicus) cattle, Java Ongole (Bos indicus) cattle, Friesian (Bos taurus) cattle, and buffaloes (Bubalus bubalis) exhibited clinical changes and lesions consistent with those detected in Bali cattle with Jembrana disease but were markedly less severe than in Bali cattle. The results confirmed previous epidemiological evidence that the disease has a predilection for and exhibits host-specificity for Bali cattle but indicated that other bovine species can be infected.
The aetiological agent exhibited characteristics of viruses in the family Retroviridae. These properties included the size, morphology and morphogenesis of the virions, the density (1.15 g/ml) in sucrose gradients, and the presence of an intravirion reverse transcriptase. The morphology and apparent morphogenesis of the virions most closely resembled viruses in the subfamily Lentivirinae. Further evidence of the relationship of the virus to lentiviruses was the antigenic relationship of an immunodominant 26K protein of the virus to the 26K capsid protein of bovine immunodeficiency virus.
An enzyme-linked immunosorbent assay (ELISA) and an agar gel immunodiffusion (AGID) test are described which detected antibody in Bali cattle (Bos javanicus) against Jembrana disease virus (JDV). The antibody response was delayed and a maximum antibody response was detected 23 to 33 weeks after infection, but persisted until at least 59 weeks after infection. The correlation between Western immunoblotting and ELISA results in individual sera indicated that the ELISA detected antibody primarily to the 26K virion protein; detection of this antibody would indicate previous infection with JDV but would not be directly correlated with the immune status of animals. The inability to detect a significant antibody response until approximately 8 weeks after infection was consistent with the absence of a significant follicular reaction and the scarcity of plasma cells in lymph nodes and spleen during the clinical and early recovery stages of disease.
There was evidence of a reduced antibody response to Pasteurella multocida and Brucella abortus vaccines in JDV-infected Bali cattle. This supported previous pathological studies that have indicated that effected cattle may have suppressed immune function, and anecdotal evidence suggesting an increased prevalence of secondary infections in cattle with Jembrana disease. An attempt to detect suppression of the cell-mediated immune response was unsuccessful.
An antibody response was detected in a majority of JDV infected Madura and Rambon (crossbred Bos javanicus) cattle, although clinical signs of disease were previously detected in only some of these cattle and the clinical signs that occurred were considerably milder than those in Bali cattle.
A serological survey detected antibody to Jembrana disease virus (JDV), the aetiological agent of Jembrana disease in Bali cattle (Bos javanicus), in cattle in 4 islands of Indonesia: Bali, Sumatra (Lampung, Sumatra Barat, Jambi and Riau provinces), Jawa (in the Banyuwangi district of Jawa Timur), and Kalimantan (Kalimantan Selatan and Kalimantan Tengah provinces). Diseases indistinguishable from Jembrana disease have been reported in all areas where antibody was detected, except Iambi, Riau and Kalimantan Tengah but the results indicated that JDV is now also present in these areas. The serological results indicated that there has been limited spread of the disease from endemic areas to neighbouring areas.
Antibodies were also detected in Ongole (Bos indicus) and crossbred Bali (Bos javanicus x Bos indicus) cattle in Lampung Tengah, and buffaloes in Bali. The presence of antibody but the lack of any evidence of disease in these animals was consistent with the experimental evidence that these cattle breeds and buffaloes can be experimentally infected with JDV but develop only a mild or subclinical disease that would be difficult to detect under field conditions.
A series of vaccination experiments were conducted which demonstrated it was possible to induce a protective immune response against Jembrana disease virus (JDV) in Bali cattle (Bos javanicus) by vaccination with whole virus vaccines prepared from plasma and spleen tissues of affected cattle. The results indicated that none of the vaccination procedures used completely prevented the development of clinical signs in animals challenged with 100 50% infectious doses of virus but that the optimal procedures developed did suppress the clinical signs as assessed by a reduction in the duration of the febrile period, a reduction in the duration of leukopenia, reduced severity of the histological lesions detected in the challenged animals, and no mortality. Optimal vaccination results were achieved using virus inactivated with Triton X-100 and emulsified in a mineral oil adjuvant and administered on 3 occasions at monthly intervals. It was considered probable that the use of this vaccination regime in Bali cattle under field conditions could produce a reasonable level of herd immunity.
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Roy, Mélanie. "Identification and characterization of differentially expressed genes in response to Escherichia coli and Staphylococcus aureus in bovine mammary epithelial cells and mammary gland." Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=98785.
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Bovine mammary glands respond to infection by foreign pathogens such as Escherichia coli (E. coli) and Staphylococcus aureus (S. aureus) through changes in gene expression. Monitoring the gene expression profiles will contribute to better understanding of the pathology of mastitis, and provide important selective markers for future animal breeding programs. Using cultured bovine mammary duct epithelial cells and somatic cells from infected bovine mammary glands, this study first examined the existence of Toll Like Receptors in these two systems. In cultured duct epithelial cells stimulated with E. coli LPS, both TLR 4 and 2 mRNA up regulation was detected at 2h-72h and 12h-48h respectively. For S. aureus LTA TLR 2 mRNA was up regulated at 48 and 72h whereas for TLR 4 mRNA expression up regulation was detected at 24, 48, and 72h in comparison to the Oh (p<0.05). In the case of PGN, an abundant structural component of S. aureus, the expression of TLR 2 mRNA was significant (p<0.05) at 72h whereas TLR 4 mRNA expression increased at 24, 48, and 72h. The expression of these receptors was also monitored in milk cells from cows infected with either E. coli or S. aureus. However, results obtained from the milk cells were inconclusive due to the high individual variability. Afterwards, differential gene expression profiles were monitored by the Differential Display Polymerase Chain Reaction technique in the cultured duct epithelial cells in response to E. coli and S. aureus structural components. A total of 6 candidate fragments were identified for E. coli LPS induction, whereas only one fragment was identified for S. aureus LTA induction. After LTA induction, a specific band was found to be up regulated and confirmed to be GCP-2, a chemokine involved in neutrophil recruitment. In contrast, PGN induction resulted in no change in GCP-2 levels. In different preparations of cultured duct epithelial cells both GCP-2 and IL-8 were confirmed by real time PCR to be up regulated by LTA with a significance of (p<0.01) when compared to the control cells. In the case of the E. coli identified bands, a different approach is necessary to potentially confirm the origin of these fragments. Further large scale screening of the GCP-2 and IL-8 genes in dairy cattle is necessary to test for their potential use as targets to differentiate the mastitis resistant from the mastitis prone cows.
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Boström, Lennart. "Tobacco smoking and periodontal disease : some clinical, microbiological and immunological aspects /." Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4456-3/.
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Sparrelid, Elda. "Infections in allogeneic stem cell transplanted patients : clinical and immunological aspects /." Stockholm, 2001. http://diss.kib.ki.se/2001/91-628-4840-2/.
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Shiau, Ai-Li. "Immunological aspects of hepatitis B virus core antigen and its derivatives." Thesis, University of Edinburgh, 1993. http://hdl.handle.net/1842/14415.
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The use of core antigen (HBcAg) of hepatitis B virus (HBV) to present peptide epitopes to the immune system has been shown to enhance immunogenicity of the peptide epitopes. HBcAg fused to the first 8 amino acid residues of β-galactosidase was exploited to serve as a carrier protein to present the epitopes from the S, preS_1 and preS_2 regions of HBV as its truncated C-terminus. The emergence of an HBV escape mutant carrying an amino acid substitution from glycine to arginine at amino acid residue 145 of the S domain suggests that it may be necessary to modify future HBV vaccines. The immunodominant region of HBAsAg carrying mutant sequence at amino acid residue 145 was also fused to HBcAg. These HBcAg fusion proteins were expressed in E.coli and produced in high yields, and assembled into core-like particles morphologically indistinguishable from HBcAg itself. The largest multiple fusion protein, containing a dimer of the HBs_(111-156) sequence as well as sequences from preS_1 and preS_2 regions carried a total of 165 amino acid residues attached to the C-terminus of truncated HBcAg, and could still be accommodated in core-like particles. The HBcAg fusion proteins displaced similar HBc antigenicity and immunogenicity to the full-length HBcAg. Immunisation of rabbits with the HBcAg fusion proteins elicited T-cell-proliferative responses to HBcAg, HBsAg and preS_1 peptides. The T-cell responses to HBcAg were much higher and more consistent than those to HBsAg or preS_1 peptide. The HBcAg fusion proteins induced antibodies against the corresponding peptides. The fusions carrying the immunodominant region of HBsAg, either wild-type or gly_145 mutant with arginine, glutamic acid or lysine substitution, showed HBs antigenicity in the immunoblot analysis and the antigen-capture sandwich radioimmunoassay, albeit at a lesser extent, using two antibodies with different specificity.
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Yip, Ming-shum, and 葉名琛. "Severe acute respiratory syndrome coronavirus infection of human immune cells through antibody-mediated pathway." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B46542139.
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Yim, Chi-ho Howard, and 嚴志濠. "Mechanisms of mycobacteria-induced innate responses." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B45200981.
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Wang, Xiaohui, and 王晓辉. "The role of IL-17A in modulating B cell response during influenza virus infection." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/208035.
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Interleukin-17A (IL-17A)is an important pro-inflammatory cytokine that plays a critical role in host defenses against diverse pathogens. Studies have shown that IL-17Aplays protective role against sub-lethal H1 and H3 subtypes influenza infections, but it is unclear about the role of IL-17A in the highly pathogenic H5N1 and lethal H1N1 influenza virus infection. B cell is an important effector cell type in anti-influenza immunity. Although roles of B cell in influenza infection have been extensively investigated, it is unclear whether and how IL-17AregulatesB cell response during influenza infection.
I examined the role of IL-17A against influenza infection by challengingIL-17A knockout (KO) and wild-type (WT) mice with highly pathogenic H5N1 and lethal H1N1 influenza viruses. Following challenge, IL-17AKO mice exhibited significantly lower survival rate, profoundly reduced body weight, more severe tissue damage and higher viral burden in the lung tissues. These evidences suggest that IL-17Aplays a protective role in lethal influenza infection.
To study whether IL-17Amodulates B cell response against influenza, I found that both B-1a and B-2 cells were detected in the lung tissue and pulmonary draining lymph node, Mediastinal lymph node (MedLN),as early as 2days post-infection. Meanwhile, B-1a cells predominantly contributed to the early virus-specific IgM in the respiratory tract. However, virus-specific IgM markedly reduced in IL-17A KO mice when compared with WT controls. Adoptive transfer of B-1a cells or B-1a cell-derived antibodies conferred protection in IL-17A KO mice. These results demonstrate that IL-17A plays a critical role in modulating early antibody production of B-1a cells against lethal influenza infection.
To further elucidate how IL-17A regulates B-1a cell response, I observed that B-1a cells migrated into MedLN and lung tissues during infection and underwent plasmacytic differentiation with increased antibody production in airways. IL-17A deficiency impaired these processes of B-1a cells, while intra-nasally instillation of IL-17A restored B-1a cell response by promoting both B-1a cell migration and plasmacytic differentiation. By inducing blimp-1 expression in B-1a cells in an NF-κB dependent pathway, IL-17A directly promoted plasmacytic differentiation of B-1a cells both in vivo and in vitro. Furthermore, chromatin immuno-precipitation analysis confirmed that NF-κB directly bound to the promoter of blimp-1 gene and promoted blimp-1 expression in B-1a cells following IL-17A stimulation.
To determine the functional significance of IL-17A signaling in modulating B cell response against influenza infection, I first uncovered markedly reduced B cell response, predominantly B-1a cell response in IL-17A KO mice, showing reduced local migration and impaired plasmacytic differentiation in the early stage of infection. Next, intra-nasal administration of IL-17A into IL-17A KO mice significantly restored this B-1a cell response. Moreover, I detected expression of IL-17A receptor in B-1a cells. IL-17A treatment could promote antibody production from B-1a cells by inducing blimp-1 expression in an NF-κB dependent pathway.
Taken together, these findings identify a novel role of IL-17A in actingas an immune modulator of B cell response against influenza infection, which will contribute to a fuller understanding of B cell biology and anti-viral response in host defense.published_or_final_version
Pathology
Doctoral
Doctor of Philosophy
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Elliott, Salenna R. "Lymphocyte expression of costimulator molecules in early life /." Title page, contents and summary only, 1999. http://web4.library.adelaide.edu.au/theses/09PH/09phe466.pdf.
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Hoedemaekers, Cornelia Wilhelmina Elisabeth. "Age-related resistance to experimental autoimmune myasthenia gravis immunological and neurobiological aspects /." [Maastricht : Maastricht : Universiteit Maastricht] ; University Library, Maastricht University [Host], 1997. http://arno.unimaas.nl/show.cgi?fid=5923.
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Sloan, Duncan J. "Some immunological aspects of neural transplantation to the CNS of inbred rats." Thesis, University of Oxford, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.280741.
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Maccoll, Gavin Stuart. "Functional and immunological aspects of growth hormone gene transfer into muscle cells." Thesis, University College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.326173.
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Snyder, Benjamin J. "Immunological Aspects of Muscle Injury and Regeneration in Young and Old Rats." Ohio University / OhioLINK, 2002. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1016641263.
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del, Fierro Gloria M. "Clinical, immunological and pathological aspects of experimental feline immunodeficiency virus (FIV) infection." Thesis, del Fierro, Gloria M. (1995) Clinical, immunological and pathological aspects of experimental feline immunodeficiency virus (FIV) infection. PhD thesis, Murdoch University, 1995. https://researchrepository.murdoch.edu.au/id/eprint/53477/.
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Feline immunodeficiency virus is a recently discovered feline lentivirus which clinically resembles human HIV-1 virus inducing immune dysfunction and secondary infections in cats. FIV presence has been confirmed throughout the world in domestic, feral and zoo cat populations. Older, free-roaming, diseased male cats are at the greatest risk of acquiring the infection.
There are no specific clinical signs restricted to FIV infection. However, weight loss, recurrent fever of undetermined origin, unthriftiness, inappetence, pyrexia, lymphadenopathy, anaemia, leucopenia and myeloproliferative disease have been often associated with this infection. Localised chronic progressive infections of the mouth, oral cavity, respiratory tract, skin and external ear canals, gastrointestinal tract, neurologic and renal dysfunction as well as ocular disease have also been reported. Data in this thesis confirms that cats experimentally infected with FIV and observed for up to 77 weeks postinfection display a greater tendency for more severe infection than non-FIVinfected cats. Among the FIV-infected cats, 73% had clinical disease and 27% were asymtomatic. Fever was a feature exclusively seen in 36% of FIVinfected cats in this study.
In the same cats hematologic abnormalities include relative lymphopenia, neutropenia and leucopenia in the acute stage of infection. Transient anaemias among FIV-infected cats during the acute phase of infection was also found. No hematologic abnormalities beyond the stage of early infection equivalent to the terminal stage of naturally acquired infection were found. Mortality among FIV-infected cats was 16%, and was limited to the primary stage of infection. There was no mortality in uninfected control cats.
Whilst a final or definitive diagnosis is arrived at by virus isolation, the demonstration of FIV antibodies generally establishes a conclusive diagnosis. Throughout this study, serodiagnostic methods such as ELISA, western blot and whole blood agglutination (VetRed™FIV) methods were used. Early detection was accomplished with both ELISA and VetRed™FIV. In experimentally infected cats the sensitivities and specificities of these two methods were comparable. The western blot was not as sensitive in the early phase of infection. A comprehensive field evaluation of the newly available VetRed™FIV commercial test was undertaken which demonstrated that while it was sensitive as the ELISA test, it was not as specific. This study also confirmed the high prevalence of FIV in Western Australian cats, especially mature male cats.
At the time of necropsy, FIV was successfully isolated from the bone marrow of all infected cats, but was less frequently isolated from other lymphoid organs such as the lymph node and spleen. In addition, FIV was isolated with high frequency from the salivary gland and kidney.
Since the discovery of FIV until the present time, studies on the pathogenesis of FIV have been fragmentary. One aspect of pathogenesis, the effect of FIV on lymphoid tissue was studied in depth. Lymphadenopathy was a consistent finding, which unless lymph node weights are quantified, may be overlooked clinically and at necropsy. In this study lymph node weights of FIV infected cats were twice that of uninfected controls. A regional pattern of enlargement was also apparent, where nodes not exposed to non-specific antigens from mucosal surfaces, like popliteal lymph nodes, were unequivocally enlarged because of hyperplasia. Additionally, the lymphadenopathy was present up to 77 weeks post-infection.
Histopathologic evidence of a range of mild, moderate to severe lesions in lymphoid and non-lymphoid organs was seen in this study covering a period from 12 to 77 weeks post-infection. Gross and histopathologic lesions were divided into (1) those exclusive to FIV-infected cats, (2) those seen in both infected and uninfected cats but of a greater severity in FIV-infected cats and (3) those with equal intensity in FIV-infected and uninfected cats. The principal histopathologic alterations observed in lymphoid tissues of FIV-infected cats not previously reported at the time of this study was thymic involution, while B-cell hyperplasia of the popliteal lymph nodes and spleen occurred 2-3 times more commonly in FIV-infected cats than in controls. In non-lymphoid organs, changes were myeloid hyperplasia in the bone marrow, mild to moderate inflammation in the choroid plexus and liver, severe interstitial pneumonia, severe granulomatous ileitis and FlP-associated granulomatous inflammation in multiple organs in some cats. While the most severe lesions occurred in one cat which died acutely at 12 weeks post-inoculation, lesions in cats infected from 21-77 weeks were generally mild to moderate in nature. It is apparent from this experiment that the severity of lesions is not directly influenced by the duration of infection.
In conclusion, the outstanding features of experimentally-induced FIV-infection in non-SPF cats were mild leucopenia which encompassed a lymphopenia and neutropenia, limited to the first few weeks of infection. This was accompanied by anemia. More importantly, this study established clinical signs that were exclusive to infection and some signs that occurred with more frequency and were more severe in FIV-infected cats. Significant pathological features included lymphadenopathy, which was present in all FIV-infected cats and persisted up to 77 weeks p.i. The need for quantification to establish the presence of lymphadenopathy is emphasized. In general terms FIV infection induced a widespread B-cell hyperplasia which was not limited to lymph nodes. Accompanying this B-cell hyperplasia and not previously reported was thymic involution. Finally, with respect to the presence of FIV in particular tissues, it is apparent from this work that the preferred site for viral isolation is bone marrow, wherein virus was isolated from every infected cat in these experiments. In contrast, the frequency of isolation from lymphoid tissues such as spleen and lymph node was much less frequent. The reasons for this decreased frequency of isolation were not explored in depth. However, it does suggest that there is either less virus present in these tissues or that the rescue of virus from these tissues is more difficult. A surprising feature of the virus isolation study was the high frequency of recovery of FIV from epithelial tissues such as salivary gland and kidney. This suggests that FIV resides in cells of the bone marrow and lymphoid tissues but also in epithelial cells.
The clinicopathologic, pathologic and virologic data from the experiments described herein indicate that FIV produces a mild acute disease and remains clinically silent for a comparatively long period of time. An in depth examination of the differences between the controls and the experimentally infected cats was required in this comparatively subtle infection to detect differences between them.
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Li, Suiyang. "Identification of DNA markers which are associated with egg production traits and Marek's disease resistance in chickens." Thesis, McGill University, 1998. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=35001.
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Production traits and disease resistance are believed to be under the control of many genes, i.e. quantitative trait loci (QTL). The objective of the present study was to establish a methodology for identifying DNA markers which are associated with QTL in chickens using an alternative approach to the traditional linkage analysis. A systematic screening approach was designed to search a chicken liver cDNA library for clones which revealed polymorphisms associated with traits. In the first stage of the experiment, a total of 92 cDNA clones were subjected to restriction fragment length polymorphism (RFLP) analysis. About 33% and 22% of the clones revealed DNA polymorphisms at MspI and TaqI restriction sites, respectively. Subsequently, DNA polymorphisms which responded to selection were identified by comparing RFLP frequencies in divergently selected strains of chickens. About 60% of the RFLPs responded to selection for egg production traits and/or Marek's disease (MD) resistance. Trait associations of these RFLPs were then studied by selectively genotyping individuals at the extremes of trait distributions, followed by an analysis of individuals in the entire population and statistical evaluation. Finally, RFLP regions of DNA markers were characterized and PCR assays for rapid RFLP screening were developed. DNA markers in two genes were identified and characterized by this methodology. One was a marker in the chicken mitochondrial genome which arose from a nucleotide substitution (T to C) in the NADH subunit IV gene. Statistical analysis for typing random individual samples from the strains showed that this DNA polymorphism was associated with mature body weight and egg specific gravity which is a strong indicator for egg shell thickness. Other analyzed markers were located in the chicken mitochondrial phospho-enolpyruvate carboxykinase (PEPCK-M). Using the cDNA of this gene as a probe, southern blotting revealed a highly polymorphic band pattern. Statistical analy
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Chan, Tak-mao Daniel, and 陳德茂. "Pathogenesis of systemic lupus erythematosus: interactions between anti-DNA antibodies and vascular endothelialcells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1994. http://hub.hku.hk/bib/B31981574.
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Yuan, Tingting, and 袁婷婷. "Identification of intermediate antibodies of broadly neutralizing HIV-1 human monoclonal antibody b12 and characterization of variable loops of HIV-1 envelop glycoprotein." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/196445.
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Roscioli, Tony Clinical School Prince of Wales Hospital Faculty of Medicine UNSW. "The genetic basis of veno-occlusive disease with immunodeficiency syndrome." Awarded by:University of New South Wales. Clinical School - Prince of Wales Hospital, 2007. http://handle.unsw.edu.au/1959.4/40599.
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This thesis addresses the genetic basis of a rare autosomal recessive primary immunodeficiency disorder with the characteristic additional feature of venoocclusive disease of the liver (VODI). The interest in this condition was stimulated both by the potential to identify the genetic basis of a rare immunodeficiency and the opportunity to gain an insight into the biological basis of hepatic veno-occlusive disease, a poorly understood condition that is encountered most frequently in Australia as a consequence of bone marrow transplantation. The gene responsible for VODI was identified by homozygosity mapping and DNA sequence analysis of positional candidates and was shown to be the PML Nuclear Body expressed protein Sp110. This is the first time a PML Nuclear Body protein has been shown to be involved in immunodeficiency disorder. Subsequent immunofluorescence studies of affected patient cell lines showed absence of Sp110 in patient B cells. The role of SP110 alleles in the susceptibility of bone marrow transplant patients to hepatic veno-occlusive disease was investigated using a cohort of patients from the Fred Hutchinson Cancer Center, Seattle. A SNP association study identified initial evidence for an association, but the study lacked sufficient power after correction for multiple testing. Contemporaneously, Dr Igor Kramnik published a report that the murine homologue of Sp110, Ifi75 (also termed Ipr1) was deleted in mice that were supersusceptible to infection with Mycobacterium tuberculosis. A further SNP association study was therefore performed utilising a NSW cohort of Mantouxpositive South East Asian migrants, which detected evidence that alleles of SP110 may be associated with progression of M. tuberculosis infection. Again, the limited size of this cohort precluded definitive findings.
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黎祝齡 and Chuk-ling Julian Lai. "The effects of examination stress on secretory immunity." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1993. http://hub.hku.hk/bib/B31234239.
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Lam, Suk-fun, and 林淑芬. "Serological response in SARS patients." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B45010201.
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Teng, Ooiean, and 丁瑋嫣. "Identification of CLEC5A in modulating host immune response after influenza A virus infection." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/208615.
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Human infections with influenza A virus (IAV) exhibit mild to severe clinical outcomes as a result of differential virus-host interactions. C-type lectin receptors (CLRs) are pattern recognition receptors that may sense carbohydrates, proteins, or lipids derived from infected hosts or the invading microbes including bacteria, viruses, fungi, or parasites. CLR-viral interaction may lead to increased viral entry and spread; furthermore, their interactions have been reported to trigger downstream signaling that further modulates host’s innate immune responses through the induction of pro-inflammatory cytokines. To date, DC-SIGN and DC-SIGNR have been shown to mediate IAV entry; however, the potential interactions between other human transmembrane CLRs with IAV have not yet been systematically investigated. We utilized lentiviral-based pseudoparticles expressing influenza hemagglutinin (HA) to examine the binding potential between HA and a panel of human CLRs expressed in soluble form. CLEC5A was identified as a potential interacting target with the HA proteins derived from a highly pathogenic avian H5N1 virus A/VN/1203/04 (VN1203) or a human seasonal H1N1 virus A/HK/54/98 (HK5498), albeit at different binding intensity. Applying siRNA gene silencing, we confirmed that CLEC5A did not enhance influenza entry in human monocytic U937 cells that constitutively express CLEC5A or in the lentiviral-transduced stable CHO and CHO-Lec2 cells that overly expressed CLEC5A. To investigate downstream signaling upon engagement of CLEC5A to influenza virus, M-CSF or GM-CSF differentiated human macrophages with high expression levels of CLEC5A and DAP12, a known adaptor protein for CLEC5A upon phosphorylation to initiate signal transduction, was subjected to CLEC5A siRNA gene silencing followed by infection with recombinant A/PR/8/34 virus expressing HA and NA derived from either VN1203 (H5N1) or HK5498 (H1N1) viruses. RG-PR8xVN1203HA,NA (H5N1) exhibited a higher infectivity and induced higher levels of pro-inflammatory cytokines (TNF-( and IFN-α) and chemokines (IP-10, MCP-1, MIG and MIP-1α) secretion in M-CSF or GM-CSF differentiated macrophages while compared to that of the RG-PR8xHK5498HA,NA (H1N1) virus. Knocking-down CLEC5A in macrophages led to a universal reduction of cytokines and chemokines secretion after infection with either the RG-PR8xVN1203HA,NA, RG-PR8xHK5498HA,NA, RG-A/VN/1203/04 (H5N1) or A/Shanghai/2/2014 (H7N9) viruses, suggesting that CLEC5A plays a role as cytokine and chemokine amplifier after influenza infection. Since DAP12 phosphorylation is known to activate downstream signaling via Spleen tyrosine kinase (Syk), pre-incubation of M-CSF macrophages with a Syk inhibitor (Bay 61-3606) also lead to a significant reduction of TNF-α and IP-10 in infected macrophages. A higher mortality was observed in CLEC5A-/- mice while compared to the wild-type C57BL/6 mice after challenged with a lethal dose of RG-A/VN/1203/04 (H5N1) influenza virus suggesting that CLEC5A as a host innate response amplifier play a protective role upon influenza infection. In conclusion, we have identified CLEC5A as a novel host factor for influenza pathogenesis by modulating host innate inflammatory response.published_or_final_version
Public Health
Doctoral
Doctor of Philosophy
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Yun, Peter Lok Wai. "Disruption Of Cell-Mediated Immune Responses By Gingipains From Porphyromonas Gingivalis." Thesis, The University of Sydney, 2001. http://hdl.handle.net/2123/4966.
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