Dissertations / Theses on the topic 'Immune system'
To see the other types of publications on this topic, follow the link: Immune system.
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the top 50 dissertations / theses for your research on the topic 'Immune system.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Browse dissertations / theses on a wide variety of disciplines and organise your bibliography correctly.
1
Vauleon, Elodie. "Implications des gènes immuns et des cellules immunes dans le glioblastome." Thesis, Rennes 1, 2013. http://www.theses.fr/2013REN1B005/document.
Full textAbstract:
Introduction : Le glioblastome (GBM) est la tumeur cérébrale primitive la plus fréquente et la plus grave de l’adulte. Des études épidémiologiques ont mis en évidence que les antécédents d’allergie sont un facteur protecteur, soulignant le possible impact de l’immunité sur le GBM. Plusieurs études transcriptomiques ont également mis en évidence des signatures immunes plus ou moins associées à la survie. Matériel et méthodes : Pour clarifier ce lien et déterminer quels gènes immuns étaient les plus impliqués dans le GBM, nous avons étudié l’expression de 791 gènes immuns dans des échantillons de GBM et de cerveaux normaux. Les interactions entre les gènes immuns ont été étudiées par une analyse de co-expression. Nous avons ensuite recherché une association entre les gènes immuns et la survie selon 3 méthodes statistiques, avant d’établir un modèle de risque mathématique validé sur plusieurs jeux de données. Enfin, nous avons étudié les cellules immunes infiltrantes sur des échantillons de gliomes dont 73 GBM par cytométrie de flux. Résultats : Un profil d’expression génique différent significativement entre le cerveau normal et le GBM a été établi de manière robuste, mais pas au sein des GBM. L’analyse de co-expression a mis en évidence 6 modules dont 5 sont enrichis en gènes ayant un lien avec la survie. Cent huit gènes immuns ont une association significative avec la survie et un prédicteur de risque à 6 gènes immuns a permis de distinguer deux groupes de patients en fonction de leur survie, y compris chez les patients dont la tumeur a un promoteur MGMT méthylé et dans le sous-groupe de GBM proneuraux. Enfin, nous avons mis en évidence, dans tous les échantillons de GBM analysés, une infiltration leucocytaire par des cellules macrophagiques/microgliales et parfois par des cellules lymphocytaires ou granulocytaires. L’infiltration de lymphocytes uniquement est associée significativement avec la survie dans notre cohorte. Conclusion : Des gènes, impliqués dans diverses fonctions immunes, sont différentiellement exprimés entre le cerveau normal et le GBM et au sein des GBM. Un prédicteur à 6 gènes robuste a été établi, il sépare les patients en 2 groupes bas et haut risque y compris ceux ayant un bon pronostic. Nous avons enfin mis en évidence dans une série de GBM une infiltration de cellules immunes, dont une infiltration lymphocytaire associée positivement à la survieBackground: Glioblastoma is the most common and lethal primary brain tumor in adults. Epidemiological studies have revealed that a history of allergies is a protective factor, thereby underlining the likely impact of the immune system on GBM. A number of transcriptomic studies have also identified immune signatures more or less associated with patient survival. Methods: In order to clarify and identify which immune-associated (IA) genes were the most involved in GBM, we studied the expression of 791 immune genes in GBM and normal brains samples. Interactions between IA genes were studied through an analysis of co-expression network. We then searched for a link between IA genes and patient survival according to 3 statistical methods, before defining a mathematical risk model based on different data sets. Finally, we studied the infiltrative immune population of 73 GBM by cytometry. Results: A significantly different profile of IA genes expression between healthy brains and GBM was consistently defined, but not among GBM. The analysis of co-expression network revealed 6 modules, 5 of which were enriched by genes associated with patient survival. 108 IA genes have a significant association with patient survival and the 6-IA gene risk predictor allowed us to distinguish two groups of patients according to their survival, including patients whose tumor had a methylated MGMT gene promoter and in the subset of proneural GBM. Finally, in every analyzed GBM sample, we have shown that there was a leukocyte infiltration by macrophages/microglial cells and sometimes by lymphocytes or granulocytes. Only the lymphocytes infiltration was significantly associated with the survival in our group of patients. Conclusion: IA genes that are involved in various immune functions are expressed differentially between healthy brains and GBM and amongst GBM. A robust 6-IA gene risk predictor was defined: it divides patients into two low and high risk groups, including those who have a good prognosis. Finally, we revealed an infiltration of immune cells in a series of GBM, only the lymphocytic infiltration was positively associated with patient survival
2
Tan, Lee Aun. "Immune system interactions with phospholipids." Thesis, University of Oxford, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.404272.
Full text
3
Degabriele, Robert, University of Western Sydney, and of Informatics Science and Technology Faculty. "Stress and the immune network." THESIS_FIST_XXX_Degabriele_R.xml, 1999. http://handle.uws.edu.au:8081/1959.7/406.
Full textAbstract:
The clonal selection/defence paradigm appears unable to reconcile immune function with homeostatic activity whereas organismic homeostasis is central to immune function in the network/autopoiesis paradigm. The aim of this investigation, therefore, was to test the proposition that immune function, that is not clonally driven (central immune system activity), contributes to organismic homeostasis in collaboration with psychoneural responses. In one experiment sheep were confined, either in groups or individually, and the time course of changes in cortisol levels, behaviour and T lymphocyte numbers were monitored. In another study, soldiers were monitored during the stressful experience of recruit training. The combined results suggest that, at least when the immune response is not clonally driven, the psychoneural system and the central immune system may not be operating independently of each other but rather as sub-networks of the organismic network. Consequently, homeostasis is properly characterised as a property of the whole organism. In autopoietic terms, then, homeostasis could be defined as the maintenance of network stability.Doctor of Philosophy (PhD)
4
Howard, Jane Katherine. "Leptin, starvation and the immune system." Thesis, Imperial College London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.396338.
Full text
5
林衛華 and Wai-wa Lam. "Multi-agent based human immune system." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1999. http://hub.hku.hk/bib/B31221117.
Full text
6
Alhajoj, Sahal Abdulaziz Mohamed. "Anti-glucocorticoids and the immune system." Thesis, University College London (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.299490.
Full text
7
Palmer, William Jack Philip. "Immune system evolution in arthropod genomes." Thesis, University of Cambridge, 2015. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.709120.
Full text
8
Joshi, Ayush. "The germinal centre artificial immune system." Thesis, University of Birmingham, 2017. http://etheses.bham.ac.uk//id/eprint/7532/.
Full textAbstract:
This thesis deals with the development and evaluation of the Germinal centre artificial immune system (GC-AIS) which is a novel artificial immune system based on advancements in the understanding of the germinal centre reaction of the immune system. The key research questions addressed in this thesis are: can an artificial immune system (AIS) be designed by taking inspiration from recent developments in immunology to tackle multi-objective optimisation problems? How can we incorporate desirable features of the immune system like diversity, parallelism and memory into this proposed AIS? How does the proposed AIS compare with other state of the art techniques in the field of multi-objective optimisation problems? How can we incorporate the learning component of the immune system into the algorithm and investigate the usefulness of memory in dynamic scenarios? The main contributions of the thesis are: • Understanding the behaviour and performance of the proposed GC-AIS on multiobjective optimisation problems and explaining its benefits and drawbacks, by comparing it with simple baseline and state of the art algorithms. • Improving the performance of GC-AIS by incorporating a popular technique from multi-objective optimisation. By overcoming its weaknesses the capability of the improved variant to compete with the state of the art algorithms is evaluated. • Answering key questions on the usefulness of incorporating memory in GC-AIS in a dynamic scenario.
9
Young, G. R. "Endogenous retroviruses and the immune system." Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1404381/.
Full textAbstract:
Initial sequencing of the human and mouse genomes revealed that substantial fractions were composed of retroelements (REs) and endogenous retroviruses (ERVs), the latter being relics of ancestral retroviral infection. Further study revealed ERVs constitute up to 10% of many mammalian genomes. Despite this abundance, comparatively little is known about their interactions, beneficial or detrimental, with the host. This thesis details two distinct sets of interactions with the immune system. Firstly, the presentation of ERV-derived peptides to developing lymphocytes was shown to exert a control on the immune response to infection with Friend Virus (FV). A self peptide encoded by an ERV negatively selected a significant fraction of polyclonal FV-specific CD4+ T cells and resulted in an impaired immune response. However, CD4+ T cell-mediated antiviral activity was fully preserved and repertoire analysis revealed a deletional bias according to peptide affinity, resulting in an effective enrichment of high-affinity CD4+ T cells. Thus, ERVs exerted a significant influence on the immune response, a mechanism that may partially contribute to the heterogeneity seen in human immune responses to retroviral infections. Secondly, a requirement for specific antibodies was shown in the control of ERVs. In a range of mice displaying distinct deficiencies in antibody production, products from the intestinal microbiota potentially induce ERV expression. Subsequent recombinational correction of a defective murine leukaemia virus (MLV) results in the emergence of infectious virus. In the long term, this leads to retrovirus-induced lymphomas and morbidity. ERVs, therefore, provide a potential link between the intestinal microbiota and a range of pathologies, including cancer. Finally, a new computational tool, REquest, was developed for use in the above studies. REquest allows the mining of retroelement (RE) and ERV expression data from the majority of commercially available human and murine microarray platforms and allows rapid hypothesis testing with publicly available data.
10
McGlasson, Sarah Louise. "Regulation of the innate immune system." Thesis, University of Edinburgh, 2015. http://hdl.handle.net/1842/17911.
Full textAbstract:
The innate immune system is the first line of defence against pathogen invasion. The range of diseases that are caused by deficiencies in or deregulation of the innate immune system illustrates the importance of maintaining an effective balance between clearance of infectious agents and minimisation of inflammatory mediated tissue damage. This thesis explores the role of two proteins in the regulation of the innate immune system. Primarily, this work investigates the effect of human β-defensin 3 (hBD3) on the response to self-DNA and pathogenic DNA. HBD3 is an antimicrobial peptide (AMP), which has been shown to have a role in regulating the immune response; increased copy number of the region containing the gene for hBD3, DEFB103, is linked to an increased risk of psoriasis. Additionally, a similar cationic AMP, LL37, has been shown to exacerbate the pathogenesis of psoriasis by forming an immunogenic complex with self-DNA. This lead to the hypothesis that hBD3 may also affect the innate immune response to DNA. Therefore this project investigates what effect hBD3 has on the response of the innate immune system to self and pathogenic DNA. Flt-3 dendritic cells were used to show that whilst hBD3 increased cellular uptake of self-DNA, it did not convert self-DNA into an immune stimulus. However, hBD3 significantly exacerbated the response to bacterial DNA in a TLR9-dependent manner, also by increasing cellular uptake into FLDCs. The finding that hBD3 increased cellular uptake of both self- and pathogenic DNA suggests that at sites of infection or increased cell death, where DNA would be found in the extracellular environment, hBD3 may increase uptake into immune cells and could induce an increased immune response. Since increased hBD3 expression is induced by inflammatory stimuli, this process would cause a positive feedback loop of inflammation during bacterial infections. In conclusion, hBD3’s role in regulating the innate immune response to DNA is at the ligand-receptor level rather than affecting signalling pathways. Furthermore, hBD3 promotes the innate immune response to bacterial DNA by increasing the efficiency of cellular uptake possibly by inducing DNA aggregation. These results implicate a possible role for hBD3 in the earliest stages of psoriatic plaque development, which is often initiated or exacerbated by an infection, and this could be investigated further. Secondly, I investigated the innate immune function of an E3 ubiquitin ligase (E3L) not previously associated with human disease. Mutations in E3L have been identified in three microcephalic primordial dwarfism families; these patients also presented with recurrent respiratory illnesses. E3L has been implicated in the regulation of the innate immune system via interactions with signalling pathways downstream of the receptor, though its role is not clear. We hypothesised that E3L had a dual role both in regulating growth and cell division and in regulating the immune system. Primary patient fibroblasts did not demonstrate an altered cytokine response to bacterial or viral ligands, implying that E3L may have a specific function in immune cells. To investigate this further, and to provide a system to study E3L in vivo, two transgenic mouse lines were designed and engineered, firstly a conditional ‘knock-out’ designed to replicate some of the alternative isoforms of E3L seen in RT-PCRs, and secondly a ‘knock-in’ line to recapitulate the human mutation in exon 7 of E3L, R185X. These mouse lines should offer an insight into the developmental role for E3L, and contribute to establishing a potential role for E3L in the innate immune system. This thesis exemplifies the complexity of the innate immune system and the regulatory pathways that interact to maintain a delicate homeostasis preventing pathogenic inflammation. Understanding these regulatory mechanisms may shed light on the pathogenicity of diseases and identification of potential targets for therapeutics.
11
Liu, Yuhong. "Sigma Receptors and the Immune System /." The Ohio State University, 1995. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487930304687004.
Full text
12
Lam, Wai-wa. "Multi-agent based human immune system /." Hong Kong : University of Hong Kong, 1999. http://sunzi.lib.hku.hk/hkuto/record.jsp?B2093337X.
Full text
13
Ozdurak, Rabia Hurrem. "Exercise Induced Endocannabinoid And Immune System Alterations." Phd thesis, METU, 2009. http://etd.lib.metu.edu.tr/upload/12611362/index.pdf.
Full textAbstract:
Endocannabinoid and immune system alterations at moderate (18 m/min)
and endurance (32 m/min) exercise intensities were assessed and compared to
controls. Rats were exercised for 60 minutes/day, 5 days/week for 16 weeks.
Immune effector cell proportions (T cell subtypes, B cells, NK cells, and
neutrophils) and endocannabinoid serum levels were determined. Anandamide
(ANA) and 2 arachidonyl-glycerol (2-AG) serum levels increased with
endurance type of exercise. mRNA expression of the CB1 receptor increased
together with ANA in the same group. Apoptotic index increased while immune
effector cells responded divergently. B lymphocyte percentage decreased while
T lymphocyte and NK cell percentage increased in blood. CD8+ subtypes
increased whereas CD11b+ cell and CD25+ cell numbers decreased in the spleen
in the endurance type of exercise group.
Rats were grouped as the control, the endurance type of exercise, the
AM281 (CB1 receptor antagonist) and the AM281+AM630 (CB2 receptor
antagonist) groups in the second part of the study. Flow cytometry and
microarray analyses of the spleen and the thymus were conducted. Endurance
type of exercise associated significantly to immunological changes particularly
to that of the T lymphocytes. T lymphocytes increased whereas cytolytic T
lymphocytes decreased in blood. T cell and double positive T cell percentages
significantly increased in the spleen. Activated T cells and NK like T cells furthermore decreased in the spleen. AM281 and/or AM630 could partially
reverse the effect of exercise in blood but not in the spleen. Alterations in the
thymus were not observed. Exercise altered 302 genes, some of them related
with the immune system. Up-regulation of heat-shock protein coding genes was
the most significant ones.
14
Negi, Pallav. "Artificial Immune System based urban traffic control." Texas A&M University, 2003. http://hdl.handle.net/1969.1/5764.
Full textAbstract:
Borrowing ideas from natural immunity, Artificial Immune Systems (AIS) offer a novel
approach to solving many diagnosis, optimization and control problems. In the course of
this research this paradigm was applied to the problem of optimizing urban traffic. The
traffic was micro-simulated with each car on a two junction road system modeled
individually. The cars themselves were programmed with 'personalities' to better
simulate real traffic. A novel AIS was developed to detect, predict, and control
anomalous traffic conditions. It was also used to optimize the flow of traffic through the
road network. Benchmarking was performed against the well accepted TRANSYT
traffic control system. Though the TRANSYT system performed better initially, the AIS
control showed marked improvement over time as it adapted better to changing traffic
conditions. This change was expected as TRANSYT is optimized for specific initial
conditions unlike the AIS system which adapts to changes.
15
Hassan-Zahraee, Mina. "Anergy and the human skin immune system." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ29956.pdf.
Full text
16
Hassan-Zahraee, Mina. "Anergy and the human skin immune system." Thesis, McGill University, 1996. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=42051.
Full textAbstract:
An initial study comparing cytokine gene expression in the skin of control vs. anergic patients lacking delayed type hypersensitivity reactivity revealed no difference; but disclosed an apparent absence of detectable CD3+ T cells in the skin of anergic individuals. To assess its significance for anergy, an investigation of the role of skin T cells in DTH-reactive healthy individuals was undertaken. To do so, the phenotypic and functional characteristics of T cells isolated from skin and blood were compared. Analysis by flow cytometry has shown that 74% of skin T cells expressed cell surface HLADR, 66% were positive for the IL-2 receptor CD25, and less than 43% have displayed the VLA integrin $ alpha$4 chain as compared to 28%, 7%, 79% for peripheral blood mononuclear cells respectively. The expression of a cutaneous lymphocyte antigen (CLA) was 61% in the former and 14% in the latter. Functionally, skin T cells failed to proliferate in response to all ligands including IL-2, anti-CD3, lectins and phorbol esters with ionomycin, as well as showed a reduced Ca++ flux to phytohemagglutinin. Skin tissue co-cultured with autochtonous PBL could inhibit its proliferative reaction. Despite their ability to proliferate, lymphocytes from skin were shown to be able to produce IFN$ gamma$ in response to PHA+IL-12 as well as anti-CD3+IL-2. Inhibition by anti-cytokine mAbs revealed that in both instances IL-12 was obligatory for this production. In an additional study it was established that a hitherto uncharacterized subset of T cells in blood which could secrete IFN$ gamma$ consisted of CLA+ cells. This observation established a functional link between these CLA+ skin-seeking T cells and the CLA+ T cells in skin.A major difference between IFN$ gamma$-producing cells from blood and skin was found to be the tempo of synthesis: whereas, PBMC was first detected to contain IFN$ gamma$ 42 hours following activation, lasting for days, skin cells were positive after 2.5 hrs of activation, (or 16x faster) for a duration of only 90 minutes. These kinetics were confirmed using intact skin in culture. Experiments designed to reveal the mechanism of this fast action have shown that mRNA for IFN$ gamma$ is present in unstimulated isolated skin T cells as well as in intact skin, but not in PBMC, and its presence may be attributed to ongoing constitutive transcription. Activation of skin T cells, which has been shown to elicit prompt translation in IFN$ gamma$ synthesis has also been shown, at the same time, to terminate IFN$ gamma$ gene transcription in an apparently selective manner. Accordingly, it can be seen that the amount of IFN$ gamma$ synthesized in skin and the duration of its synthesis is preprogrammed. This mode of regulation may be unique to the skin, and unique for IFN$ gamma.$
The results presented are interpreted to indicate that r cells present in human skin may play an essential role in the DTH response, and provide evidence for "peripheral sensitization", or lymphocyte activation outside organized lymphoid tissue. Because of its speed, it may represent the antigen-specific component of a first line cutaneous host defence system. The absence of such T cells in the skin of anergic patients may indeed be responsible for a lack of DTH reactivity, and its clinical consequences.
17
Wodarz, Dominik. "Mathematical models of virus immune system interactions." Thesis, University of Oxford, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.268104.
Full text
18
Chan, S. S. M. "Interactions of Salmonella with the immune system." Thesis, University of Cambridge, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.597422.
Full textAbstract:
Live attenuated Salmonella that express heterologous antigens are attractive vehicles for the presentation of antigens for systemic and mucosal immunity. It is hypothesised that this requires uptake and interaction with DCs although this has yet to be studied in large animal models. This study has used pseudoafferent cannulated sheep to provide physiologically relevant DCs. However, in many other systems in vitro derived DCs are used in studies with Salmonella. Therefore we have cloned and expressed ovine IL-4 and developed protocols for derivation of in vitro generated DCs from comparison with this data. Cannulation of pseudoafferent and efferent lymphatics further allows monitoring of the earliest events of an in vivo Salmonella infection. Following in vitro infection with S. abortus ovis (a sheep specific Salmonella serotype) very few DCs were found to contain intracellular Salmonella. Avirulent Salmonella mutants were rapidly cleared from afferent lymph DCs in vitro unlike their virulent parental strains, which were found to survive and replicate intracellularly. Despite the rapid clearance of attenuated S. abortus ovis mutants from DCs, Maedi Visna virus (MVV) gag antigens expressed in these Salmonella were found to be presented to T cells. Following subcutaneous injection of aroA- S. abortus ovis expressing MVV gag p25, Salmonella were found in the afferent lymph and cells draining the infection site. However, no bacteria were detected in the efferent lymph or cells. Phenotypic changes indicative of enhanced DC maturation in afferent lymph as well as lymphocyte activation in afferent and efferent lymph were also observed. Functional anti-Salmonella immune responses in efferent lymph were also studied. This study has established that Salmonella can infect afferent lymph dendritic cells of a large animal model. Such cells migrate to the lymph node where they initiate immune responses and can influence the cells' activation and the immune mechanisms invoked.
19
Hamdan, Suhail A. El-Ghani. "The neuropeptide ACTH and the immune system." Thesis, University of Strathclyde, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.366747.
Full text
20
Smith, Carine. "Exercise, stress and immune system functional responses." Thesis, Stellenbosch : University of Stellenbosch, 2004. http://hdl.handle.net/10019.1/16070.
Full textAbstract:
Dissertation (PhD)--University of Stellenbosch, 2004.ENGLISH ABSTRACT: Stress related to chronic exercise affects both the immune and endocrine systems, but there are still many issues that are poorly understood, particularly effects of stress on the functional capacity of immune cells. This thesis probed some of these issues using physiological models of physical and psychological stress. Both exercise training stress and chronic psychological stress in human subjects were shown to result in an up-regulation of spontaneous reactivity of white blood cells in vitro, using two different assays, namely a) a peripheral blood mononuclear cell (PBMC) culture assay measuring immune cell responsiveness and b) a relatively new flow cytometry technique for assessing activation status of cells by their expression of the surface marker CD69, in a lymphocyte subpopulation-specific manner. An up-regulation of immune cell activation in the absence of an additional stressor was associated with a decreased capacity to mount a response to a subsequent mitogen stimulus in vitro after chronic psychological stress and acute, extreme exercise stress. Another novel finding was that cortisol high-responders to chronic psychological stress exhibited a higher spontaneous reactivity of both CD4+ and CD8+ lymphocytes when compared to cortisol low-responders. This result indicates that chronic exposure to cortisol may decrease its usual inhibitory effect on spontaneous T lymphocyte responsiveness. After optimisation of an animal model of mild, psychological stress, we demonstrated (using an IL-6 antibody) that IL-6 is necessary for a full-blown cortisol response to chronic, intermittent mild stress. Results also suggest that IL-6 plays a role in regulation of its own secretion by PBMCs in response to a stressor, by maintaining the production of IL-1β in the face of stress. Basal serum corticosterone concentration was shown to be the main determinant of the magnitude of mitogen-stimulated PBMC secretion of IL-6 in vitro in the stress-free controls. However, after blocking of IL-6 in vivo, IL-1β was identified as a major regulator of IL-6 secretion by mitogen-stimulated PBMCs in vitro, independently of the presence or absence of stress. The implications of these novel findings are that proinflammatory cytokines are sensitively regulated during mild stress.Mean serum cortisol concentration at rest was not a useful tool to assess chronic exercise stress after training intervention. However, classification of athletes at baseline into two groups according to their resting serum cortisol concentration illustrated two distinct patterns for the responses of both cortisol and the cortisol:testosterone ratio to chronic stress. These studies on the effects of chronic stress on parameters of the endocrine stress-axis and the immune system led to the following main conclusions: a) chronic exposure to cortisol results in a decreased inhibition of spontaneous immune cell activity at rest, b) this increased spontaneous activation of immune cells at rest in the absence of a stressor, is associated with a suppression of immune capacity to respond to a subsequent challenge, c) the latter finding is not evident under stress-free conditions where cortisol promoted immune cell IL-6 secretion, and d) IL- 1β and IL-6 are involved in the regulation of each others’ secretion.
AFRIKAANSE OPSOMMING: Chroniese oefening-verwante stres beïnvloed beide the immuun- en endokriene sisteme, maar daar is nog baie aspekte wat swak begryp word, veral m.b.t. die effekte van stres op die funksionele kapasiteit van immuunselle. Hierdie tesis het sommige van dié vraagpunte ondersoek deur gebruik te maak van fisiologiese en psigologiese stres. Beide oefening program-verwante stres en chroniese psigologiese stres in proefpersone het ‘n op-regulering van spontane witbloedselreaktiwiteit in vitro tot gevolg gehad, wat d.m.v twee verskillende metodes aangetoon is, naamlik a) ‘n perifere bloed mononukluêre selkultuur (PBMS-kultuur) bepaling van immuunsel reaktiwiteit en b) ‘n relatief nuwe vloeisitometriese tegniek vir die assessering van aktiveringsstatus van selle, deur hul uitdrukking van die oppervlakmerker CD69, op ‘n limfosiet subpopulasie-spesifieke wyse. ‘n Opregulering van immuunselaktiwiteit in die afwesigheid van ‘n addisionele stressor is geassosieer met ‘n verlaagde kapsiteit om te reageer op ‘n latere mitogeniese prikkel in vitro, na chroniese psigologiese stres en akute, erge oefeningstres. Nog ‘n nuwe bevinding was dat kortisol hoog-respondeerders, in reaksie op chroniese psigologiese stres, ‘n hoër spontane reaktiwiteit van beide CD4+- and CD8+-limfosiete toon in vergelyking met kortisol laagresopndeerders. Hierdie bevinding toon aan dat chroniese blootstelling aan kortisol die inhiberende effek daarvan op spontane reaktiwiteit van T-limfosiete verminder. Na optimalisering van ‘n rotmodel van gematigde, psigologiese stres, het ons gedemonstreer (deur gebruik te maak van ‘n IL-6 teenliggaam) dat IL-6 nodig is vir ‘n volledige kortisolreaksie op chroniese, onderbroke, gematigde stres. Die resultate dui daarop dat IL-6 ‘n rol in die regulering van sy eie sekresie deur PBMSe in reaksie tot ‘n stressor speel, deur die handhawing van produksie van IL-1β in die teenwoordigheid van stres. Basale serum kortisolkonsentrasie is as die belangrikste beslissende faktor in die omvang van mitogeengestimuleerde PBMS sekresie van IL-6 in vitro in die stresvrye kontroles aangedui. Na blokkering van IL-6 in vivo, is IL-1β egter as ‘n belangrike reguleerder van IL-6 sekresie deur mitogeen-gestimuleerde PBMSe in vitro geïdentifiseer, onafhanklik van die teenwoordigheid of afwesigheid van stres. Die implikasie van hierdie nuwe bevindinge is dat proinflammatoriese sitokiene tydens gematigde stres sensitief gereguleer word.Die gemiddelde serum kortisolkonsentrasie in ‘n rustende toestand was nie ‘n gepaste instrument om chroniese oefeningstres na ‘n oefenprogram-ingreep te assesseer nie. Na basislyn klassifikasie van atlete in twee groepe volgens hul rustende serum kortisolkonsentrasie, is twee afsonderlike patrone vir die reaksie van beide kortisol en die kortisol:testosteroon verhouding egter aangetoon. Hierdie studies rakende die effekte van chroniese stres op parameters van die endokriene stres-as en die immuunsisteem het tot die volgende vernaamste gevolgtrekkings gelei: a) chroniese blootstelling aan kortisol het ‘n verlaagde inhibisie van spontane immuunselaktiwiteit tydens rustende toestande tot gevolg, b) hierdie verhoogde spontane aktivering van immuunselle tydens ‘n rustende toestand word geassosieer met ‘n onderdrukking van immuunkapasiteit om te reageer op ‘n daaropvolgende prikkel, c) laasgenoemde bevinding is nie sigbaar tydens stresvrye toestande, wanneer kortisol IL-6 sekresie bevorder, nie en d) IL- 1β en IL-6 is betrokke by die regulering van mekaar se sekresie.
21
Klein, Jamie Ilana, and Jamie Ilana Klein. "A Camper's Guide to the Immune System." Thesis, The University of Arizona, 2017. http://hdl.handle.net/10150/625022.
Full textAbstract:
The purpose of this literature review is to compile research about common health events
that occur at summer camp and the associated immune system processes. By creating a link
between typical summer camp injuries, illnesses, and the resulting immune responses, this
review can educate youth, parents, and camp staff about health and safety of children attending
summer camps. Research in these areas was assembled in three ways: first, by analyzing my own
experience as a camper, counselor, and administrative team member; second, by applying
content from courses "Physiology of the Immune System" and "Infancy and Childhood
Development"; and third, by examining research previously done and posted in various journals,
books, and websites. Using the fictional camper, Calvin, he experiences four common issues;
skin abrasions, insect bites, parasite ingestion, and contact dermatitis. Skin abrasions result in
release of cytokines that stimulate an acute inflammatory response. With the activation of the
plasma-kinin and coagulation cascades, the inflammation is kept local and the wound heals.
Insect bites lead to activation of antibodies, which are able to clear countless extracellular
infections due to high variability and specificity. Similarly, a special class of antibodies,
specifically IgE, clears parasite infections. Lastly, contact dermatitis results from a type IV
immune response, in which T-helper cells react excessively. Further research is required to
report sufficient safety and preventive practices.
22
Alder, Matthew N. "The adaptive immune system of sea lamprey." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2008. https://www.mhsl.uab.edu/dt/2009r/alder.pdf.
Full text
23
Riesbeck, Kristian. "Effects of fluoroquinolones on the immune system." Malmö : Dept. of Medical Microbiology, Lund University, Malmö General Hospital, 1994. http://books.google.com/books?id=-hRtAAAAMAAJ.
Full text
24
Chen, Hao. "THE EVOLUTION OF THE ADAPTIVE IMMUNE SYSTEM." Diss., The University of Arizona, 2010. http://hdl.handle.net/10150/195455.
Full textAbstract:
Models proposed for the molecular evolution of the immune system are based on comparative studies of living species. Sharks are critical in this regard since they belong to an ancient clade (chrondrichthyans) that can be traced in the fossil record to the time of the earliest vertebrates. Approximately 450 million years ago, the gnathostomes diverged into two groups, the chondrichthyans (sharks and rays) and the osteichthyans (line leading to modern teleosts and tetrapods). It can be concluded that the molecular components of the immune system are ancient and arose prior to this divergence. This follows from studies showing that all the defining elements of the immune system, antibodies, T cell receptors (TCRs), MHC products and recombination activator genes (RAG), are present in chondrichthyes (4, 5). Thus, continued studies of sharks and rays, the most distant living relatives of mammals with a vertebrate type (VDJ-C recombination) immune system, should provide insights into the molecular origins and evolution of the immune system.In this research, 1) I report the sequence of the sandbar shark TCR gamma chain genomic locus and confirm that it has a prototypical translocon arrangement. 2) I also show that in the sandbar shark TCR gamma V regions undergo somatic hypermutation, in addition to DNA recombination and junction addition and deletion, to generate TCR diversity.3) Ireport the sequence of the sandbar shark beta-2 microglobulin (b2m)genomic locus.These findings certainly have functional implications for gamma/delta T cells, b2m and MHCs in sharks, and may have phylogenetic significance for understanding the evolutionary origins of diversity in the immune system.
25
Ong, Arlene. "An adaptive anomaly detection system using data mining and an artificial immune system." Thesis, King's College London (University of London), 2007. https://kclpure.kcl.ac.uk/portal/en/theses/an-adaptive-anomaly-detection-system-using-data-mining-and-an-artificial-immune-system(10ee489b-585b-4422-a6cd-207a92221911).html.
Full text
26
Pitchai, Manju Sofia. "Harnessing the immune response to enhance osseointegration." Thesis, Griffith University, 2022. http://hdl.handle.net/10072/418638.
Full textAbstract:
New understanding of immune system biology has led a paradigm shift in the development of biomaterials away from classically ‘inert’, to ‘immuno-modulatory’ biomaterials that have the potential to stimulate an immune response able to promote constructive and functional tissue remodeling responses as opposed to persistent inflammation and scar tissue formation. This project aims to examine macrophage behavior and in particular integrin expression at the cell–biomaterial interface in vitro, in order to delineate the underlying molecular events occurring during biomaterial-mediated osseous healing. After reviewing the current literature to identify research gaps that this thesis should focus on, the activation of macrophages with controlled timing, and modulation of their interactions with other cell types involved in wound healing, emerged as key strategies to improve biomaterial efficacy. Careful design of biomaterial structure and controlled release of immunomodulators can be employed to manipulate macrophage phenotype for the maximization of the wound healing response with enhanced tissue integration and repair, however, to elicit predictable immune responses there is a need for a thorough understanding of how the biomaterial properties can be tuned to harness a designed immunological outcome.
Our systematic review of in vitro studies suggested that the initial immune response of macrophages to titanium may be modulated by its surface characteristics both topographically and physiochemically. We therefore assessed the potential effects of three novel titanium surfaces; Machined, Blasted and Fluoride-treated, on macrophage phenotype. We chose a monocytic cell-line as our macrophage source rather than using primary macrophages, as the inflammatory status of primary cells could not be readily defined nor reproduced between experiments. This was crucial to the overall study if we were to clearly assess any changes in macrophage phenotype as a result of their II interaction with the titanium surfaces. We subsequently analysed in some detail the experimental processes involved in the optimization of macrophage cell culture, macrophage differentiation and phenotype characterization.
We used microscopy, profilometry and elemental analysis to understand how the roughness of the titanium surfaces affected macrophage viability and proliferation in both non-activated ‘M0’ and activated inflammatory ‘M1’ macrophages. Subsequent analysis of one of the key mediators of cell attachment to biomaterials showed for the first time that αM, β1, β2 and α2 integrins play an important role in the adhesion of non-polarised M0 macrophages onto both smooth and rough titanium surfaces. Moreover, the distinct temporal expression profile of αM integrin expression correlated broadly with the subsequent secretion profiles of inflammatory cytokines IL-1β and TNF-α in these cells. Specific integrin expression also played an important role in the adhesion of polarised inflammatory M1 macrophages onto surface-modified titanium surfaces. In these cells, early integrin αM and β1 in particular, along with integrin α2 was associated with modulation of the subsequent cytokine response in these cells. Furthermore, the surface induced differential expression of integrins on the different titanium surfaces showed the Fluoride-modified surface in general induced greater cytokine and integrin modulation than either the Machined or Blasted surfaces. While now biologically plausible, further studies to fully determine how integrin-derived modulation of the macrophage-associated inflammatory response following macrophage attachment as suggested by these studies, can enhance wound healing and osteogenesis are required. Despite this, ‘harnessing the immune response’ is clearly a potential goal of engineered titanium implant surfaces in order ‘to enhance osseointegration’.Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medicine & Dentistry
Griffith Health
Full Text
27
Degabriele, Robert. "Stress and the immune network." Thesis, Campbelltown, N.S.W. : University of Western Sydney, Macarthur, Faculty of Informatics, Science and Technology, 1999. http://handle.uws.edu.au:8081/1959.7/406.
Full textAbstract:
The clonal selection/defence paradigm appears unable to reconcile immune function with homeostatic activity whereas organismic homeostasis is central to immune function in the network/autopoiesis paradigm. The aim of this investigation, therefore, was to test the proposition that immune function, that is not clonally driven (central immune system activity), contributes to organismic homeostasis in collaboration with psychoneural responses. In one experiment sheep were confined, either in groups or individually, and the time course of changes in cortisol levels, behaviour and T lymphocyte numbers were monitored. In another study, soldiers were monitored during the stressful experience of recruit training. The combined results suggest that, at least when the immune response is not clonally driven, the psychoneural system and the central immune system may not be operating independently of each other but rather as sub-networks of the organismic network. Consequently, homeostasis is properly characterised as a property of the whole organism. In autopoietic terms, then, homeostasis could be defined as the maintenance of network stability.
28
Piani, Daniela. "Immune-mediated cytotoxicity in the central nervous system /." [S.l.] : [s.n.], 1993. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=10423.
Full text
29
Vale, Julie Racquel. "The human immune system a challenging control problem /." Waterloo, Ont. : University of Waterloo, 2004. http://etd.uwaterloo.ca/etd/jrvale2004.pdf.
Full textAbstract:
Thesis (M.A.Sc.) -- University of Waterloo, 2004."A thesis presented to the University of Waterloo in fulfilment of the thesis requirement for the degree of Master of Applied Science in Electrical and Computer Engineering". Includes bibliographical references.
30
Vale, Julie. "The Human Immune System: A Challenging Control Problem." Thesis, University of Waterloo, 2004. http://hdl.handle.net/10012/858.
Full textAbstract:
This work deals with the control of the human immune system. A standard immune system model is modified by introducing control signals corresponding to drug cocktail and immune suppressor treatments. The ultimate objective is to use these control signals to 'cure' a chronically-ill patient. Control is challenging for this system due to nonlinearities and time delays. In fact, it is shown that fundamental aspects of the system dynamics are lost when the system is linearised; hence, control approaches involving linearisation are fruitless. Feedback linearisation and some optimal control methods are also investigated and shown to be infeasible. However, it is shown that, for certain parameter values and initial conditions related to the virus and patient, a specific open-loop control scheme using only the drug cocktail achieves the objective. It is also proven that, unfortunately, this control scheme fails for other parameter values and initial conditions. A two-stage open-loop controller that uses both control inputs is then proposed. It is shown in simulation that the two-stage controller works over a larger set of parameters and initial conditions than the single-stage controller, but a rigorous analysis of the two-stage controller remains elusive.
31
Kasiewicz, Lisa N. "siRNA Loaded Lipidoid Nanoparticles and the Immune System." Research Showcase @ CMU, 2018. http://repository.cmu.edu/dissertations/1146.
Full textAbstract:
Delivery vehicles are necessary for many therapeutics to overcome the various challenges in their path. It is clear, however, that the relationship between delivery vehicles and the immune system is a complex one. One such delivery vehicle is the lipidoid nanoparticle, which has been shown to be potent in several cell types. This thesis details the first time lipidoids have been used for wound delivery, and demonstrates the successful silencing of an inflammatory protein, TNFα, in the context of diabetic ulcers. Knockdown is seen in an in vitro macrophage-fibroblast coculture model, as well as in nondiabetic and diabetic mice wound models. Lipidoids silence roughly half of the TNFα gene expression in the diabetic wound and have been shown to help the wound close faster than untreated controls. Of course, immune activation can decrease therapeutic efficacy or trigger dangerous reactions in the patient. Learning more about what chemical moieties cause an immune response would allow for the design of a particle that could better resist immune clearance and avoid the creation of a secondary response. This thesis investigated the effect of a lipidoid library on the immune system using a two pronged approach. The lipidoids were first tested against human peripheral blood mononuclear cells and then were injected into mice to probe the in situ immune response. Several types of B cells were examined in this latter case, namely germinal center B cells, plasma cells, and memory B cells. A T cell dependent response occurred, favoring memory B cells for most of the lipidoids tested. There was an increase in free antibody in the blood that reflected this increase in antibody producing cells. Nitrogen rings and carbon tail lengths of eleven and twelve carbons were particularly reactive, though it appears that the amine head group determines immune response more than the tail. Further work will analyze whether these increases in immune cells reflect a loss of therapeutic efficacy, as current ramifications are unclear. An in-depth T cell subset analysis with flow cytometry would also help complete the picture.
32
Sustackova, Helena. "The role of the immune system in arthritis." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq28067.pdf.
Full text
33
Dionissopoulos, Louis. "Immune system stimulation and growth performance in swine." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ35883.pdf.
Full text
34
Aloyouni, Sheka Yagub. "Modulation of the immune system by Listeria monocytogenes." Thesis, University of British Columbia, 2013. http://hdl.handle.net/2429/44394.
Full textAbstract:
We had previously shown that attenuated Listeria monocytogenes (Lm) vaccines induce a strong Th1 response in neonatal mice, and prophylactically protect against histopathological signs of asthma.
To test the ability of Lm as a therapeutic vaccine to diminish allergic sensitization in a mouse model of ovalbumin (OVA)-induced asthma, adult mice were sensitized intraperitoneally and challenged intranasally with OVA to induce asthma. Mice were then immunized intraperitoneally with a single dose of either live attenuated Lm vaccine that expresses OVA (LmOVA), live Lm expressing no allergen, or NaCl. Six weeks later, anesthetized mice were challenged intranasally with OVA and evaluated for cellular infiltration and tissue remodeling. We found that vaccination with live-attenuated Lm strains did not reduce already established allergic inflammation in all of the parameters we measured except that it did significantly reduce the total BALF eosinophil count in the LmOVA group.
To test the functional impact of our prophylactic vaccine approach in vivo, we immunized mice as newborns with live LmOVA or Lm, followed 6 weeks later by allergic sensitization with OVA and evaluation by FlexiVent to determine airway hyperreactivity. We found that prophylactic vaccination reduced airway hyperreactivity, in an antigen-specific (i.e. LmOVA) as well as non-specific (i.e. Lm not expressing OVA) manner. Thus, our neonatal prophylactic vaccine approach holds promise as a powerful tool to modulate early life immune ontogeny and effectively prevent asthma.
In order to study any potentially harmful effect of neonatal immunization with Lm, newborn mice were immunized intraperitoneally with the live Lm attenuated strain or with saline. Six weeks later, anesthetized mice were challenged intranasally with Saccharopolyspora rectivirgula antigen (SR-Ag) on three consecutive days per week for three weeks. We were unable to detect any changes on the HP phenotype comparing vaccinate vs. unvaccinated mice.
In conclusion, prophylactic neonatal immunization with Lm-based vaccines provided functional protection from asthma in vivo, and may also provide some therapeutic benefit. Importantly, Lm-induced early life immune modulation did not exacerbate the development of some Th1/Th17-biased diseases later in life.
35
Mélançon, Johanne. "Modulation of the immune system by Neisseria meningitidis." Thesis, McGill University, 1986. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=72781.
Full text
36
Stekel, Dov Joseph. "Mathematical models of immune system and virus dynamics." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.364143.
Full text
37
Pichlmair, Andreas. "Recognition of viruses by the innate immune system." Thesis, University College London (University of London), 2008. http://discovery.ucl.ac.uk/1445012/.
Full textAbstract:
When a cell gets infected with a virus, the innate immune system swings into action within minutes. The rapid production of pro-inflammatory cytokines and antivirally active type-I Interferons (IFN-a/p) is the most significant mechanism to limit virus spread. Two conceptually different pathogen recognition mechanisms are known that lead to antiviral responses through production of IFN-a/p: Specialised immune cells possess Toll-like receptors (TLRs), which sense incoming viruses in endosomes. Most other cells rely on the cytoplasmic RNA-helicases RIG-I and MDA5 that sense the presence of viruses within the cell. However, although proteins and signalling networks involved in innate recognition of viruses are well known, the exact molecular details of their interactions with the virus are only marginally understood. During my PHD thesis I dedicated myself to aid our understanding of virus recognition. I could show that recombinant lentiviruses are weak inducers of IFN-ct/p* in murine immune cells. Standard preparations of lentiviral vectors, however, are strong activators of the innate immune system. This activity is contained in tubulo-vesicular structures that are present within standard lentiviral preparations and have the ability to activate TLR9. Tubulo-vesicular structures can serve as adjuvant to facilitate adaptive immune responses and may therefore be important when considering lentiviral vectors for clinical applications. In my second project I focused on cytoplasmic virus recognition. Surprisingly, viral genomic single-stranded RNA from influenza virus can activate the cytoplasmic virus recognition receptor RIG-I. Unlike most cellular RNA species, single-stranded RNA from influenza and other viruses bear a 5' triphosphate group, which marks this RNA as 'foreign' and thereby induces interferon responses. Importantly, influenza virus codes for an interferon antagonist, the non-structural protein 1 (NS1), which forms a complex with RIG-I, suggesting that influenza virus specifically interferes with this pathway. In conclusion, the innate immune system employs diverse mechanisms to sense the presence of a virus through recognising diverse forms of viral nucleic acid.
38
Campbell, Gillian Mhairi. "Influenza virus infection in a compromised immune system." Thesis, University of Edinburgh, 2012. http://hdl.handle.net/1842/6521.
Full textAbstract:
Severe influenza virus infection, including human infection with highly pathogenic H5N1 viruses is characterised by massive pulmonary inflammation, immunopathology and excessive cytokine production, a process in which macrophages may play a vital role. The aim of this project was to investigate the hypothesis that inhibition of inflammatory responses from infected macrophages, using either alternatively activated bone marrow derived macrophages (BMDMf), or IFNg receptor deficient (IFNgR-/-) mice may ameliorate the devastating immunopathology and inflammation routinely observed in highly pathogenic influenza virus infections. Infection of alternatively activated BMDMf resulted in enhanced positivity for viral proteins, compared with classically activated, inflammatory BMDMf. However, neither subset propagated the infection indicating that while infection is abortive in both classical and alternatively activated BMDMf, the latter may prove more efficient at removing infectious virus from the site of infection due to enhanced infectivity. However, influenza virus was capable of driving expression of proinflammatory mediators such as iNOS and TNFa from classical and alternatively activated BMDMf even in the absence of IFNg signalling. IFNgR-/- BMDMf demonstrated a reduced inflammatory response to infection compared to Sv129 counterparts, suggesting a potentially impaired inflammatory response in vivo. This was investigated by infection of IFNgR-/- mice, which resulted in ameliorated disease, lower viral titres and mild immunopathology, demonstrating that inhibition of IFNg signalling limits the severity of disease. Additionally, mRNA expression for key inflammatory mediators was reduced, demonstrating that inhibition of the overwhelming inflammatory response to influenza virus infection is beneficial to the host, resulting in protection from immunopathology and improved prognosis, without impairing viral clearance.
39
Campbell, David J. "Age-associated changes to the feline immune system." Thesis, University of Ulster, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.414099.
Full text
40
Thill, Peter (Peter Daniel). "Mitigating and exploiting stochasticity in the immune system." Thesis, Massachusetts Institute of Technology, 2016. http://hdl.handle.net/1721.1/105051.
Full textAbstract:
Thesis: Ph. D., Massachusetts Institute of Technology, Department of Chemistry, 2016.Cataloged from PDF version of thesis.
Includes bibliographical references.
In the adaptive immune system of higher organisms, T cells are responsible for detecting infections and mounting a response. It is of great importance that T cells respond accurately to very small traces of pathogenic signal in a background sea of healthy cells, to which mounting an immune response in the absence of viral infection could prove fatal for the organism. T cells detect pathogenic signal through noisy protein interaction networks. The goal of this work is to understand how the noise intrinsic to signal transduction mechanisms is mitigated and in some cases exploited to outperform corresponding deterministic mechanisms. Two broad areas of research are presented in this work: 1). Due to fluctuating conformations of proteins, the rate constants of various chemical reactions are not fixed but fluctuate stochastically throughout the course of a signaling cascade. For modeling purposes, this implies that signal detection is based on samples from a large, continuous-time Markov chain whose rate constants follow their own stochastic process. We seek to understand how this behavior limits the information that a network can transmit, and how these limitations can be mitigated based on the specific network topology, or exploited in biological systems to limit autoimmunity. We develop algorithms to detect and characterize the distribution that rate constants sample from. 2). The topology of very early stages in T cell signaling is critical for mounting an accurate immune response. We explore a mechanism that contrasts with the conventional signaling network topology, that outperforms the original by all metrics considered and explains recent experimental results. We study the role that stochasticity in the dwell time of a T cell at an APC plays in achieving a robust cellular response, and explore models of sequential decision making in the immune system.
by Peter Thill.
Ph. D.
41
Marshall, Sara Elizabeth Farha. "Tolerance and suppression in a primed immune system." Thesis, University of Cambridge, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.627651.
Full text
42
Davies, John Stephen. "Heterochronic Parabiosis Studies of the Aging Immune System." Diss., The University of Arizona, 2016. http://hdl.handle.net/10150/613368.
Full textAbstract:
Parabiosis is the surgical union of two organisms resulting in the development of a single, shared circulatory system. When animals of different ages are conjoined (i.e. heterochronic parabiosis), blood-borne factors from the parabionts can affect the physiology of the other parabiont. This is manifested sometimes by beneficial, rejuvenating impact upon the older animal's tissues and organs (anti-geronic effect), and sometimes by younger animal's tissues regressing and appearing old-like (pro-geronic effect). These effects, and the ability to identify individual factors that could recapitulate pro- and anti-geronic effects, have made heterochronic parabiosis a very attractive approach to studying biology of aging and rejuvenation.cHowever, heterochronic parabiosis has not been widely used to investigate the aged immune system. An important question to be answered is whether the cellular defects involved in the aged immune system are due to intrinsic defects or if they can be rescued by extrinsic factors. Heterochronic parabiosis is ideal to test cellular migration patterns, interrogate the mechanisms driving migration defects that occur with aging, establish if these defects can be rejuvenated and identify molecules that are targets for intervention. Here, we provide evidence of the importance of reducing differences in the background genetics of different C57BL/6 substrains prior to parabiosis. This improvement allowed us to improve survival and confirm robust lymphocyte equilibration across secondary, but not primary, lymphoid tissues. We found no evidence for rejuvenation of the old immune cells, whereas results suggested that adult peripheral lymph nodes (pLN) lost mass and cellularity, potentially indicating the presence of a pro-geronic factor(s) in the old circulation that affects pLN function. Adult and old immune cells were present in equal frequencies in both adult and old secondary lymphoid tissues, indicating that there was no restriction of cellular migration due to the age of the cell or age of the tissue. The propensity of adult immune cells (i.e. large naïve compartment) to occupy lymph nodes and old immune cells (i.e. large memory compartment) to occupy bone marrow was retained following heterochronic parabiosis. Finally, parabiosis separation experiments illuminated the peripheral survival advantage of old T cells over adult T cells. These results highlight the power of heterochronic parabiosis in studying immune aging and provide hypothesis-generating data for future mechanistic studies of peripheral T cell maintenance with aging.
43
Blowers, Pinar. "Immune system involvement in metal hip implant failure." Thesis, University of East Anglia, 2015. https://ueaeprints.uea.ac.uk/54300/.
Full textAbstract:
Osteoarthritis (OA) is the most common debilitating disease, especially in the elderly. Total Hip Replacement (THR) is a last resort treatment for hip OA and Metal-on-Metal (MoM) THR was used commonly for its durability. While this is an effective treatment for many, around 12% of hip implants were revised in 2012. MoM articulations had poor implant survival compared with non-MoM, displaying four times higher failure rate. Between 1997 and 2004, 652 hip replacement surgeries were undertaken in Norfolk using the Ultima TPS MoM THR system (DePuy) which resulted in a high rate of early implant failure (27.4% at year 7). One of the proposed reasons for MoM THR failure is the adverse reaction to metal wear debris and consequent immune system mediated osteolysis resulting in peri-prosthetic loosening. To understand the immune system involvement in metal hip implant failure, a cohort of OA patients were recruited with and without an Ultima implant. This study investigated; The Human leukocyte antigen (HLA) allelic variation and implant failure association. Determined the composition and frequency of immune cells and inflammatory markers in Norfolk cohort. And tested the metal particle impact on immune cells. These experimental approaches were utilised to elucidate whether the metal implant failure is a result of an inflammatory process. The genetic disposition to metal hip implant failure was tested by conducting HLA typing for 25 different alleles across three MHC class II loci which revealed a protective haplotype against implant failure being DQA1*01:02 - DQB1*06. The analysis of immune parameters showed that all patient groups had normal levels of immune cell composition and cytokine levels apart from the Ultima Asymptomatic group, suggesting a regulatory mechanism in place for metal hip implant survival. Analysis of metal particle effect on immune cells demonstrated that these particles are immune-reactive and results inmacrophage-initiated and lymphocyte-mediated failure mechanisms.
44
Дядечко, Алла Миколаївна, Алла Николаевна Дядечко, Alla Mykolaivna Diadechko, and L. Listunova. "New nano device detects immune system cell signaling." Thesis, Вид-во СумДУ, 2009. http://essuir.sumdu.edu.ua/handle/123456789/16938.
Full textAbstract:
By using new technology medical people will be able to contribute a lot to fighting immune system invaders.
When you are citing the document, use the following link http://essuir.sumdu.edu.ua/handle/123456789/16938
45
Bowman, Nicholas Spencer, and Nicholas Spencer Bowman. "The Relationship between Antibodies and the Immune System." Thesis, The University of Arizona, 2017. http://hdl.handle.net/10150/624919.
Full textAbstract:
The human body defends itself from outside pathogens through the immune system. There are two types of immunity, innate immunity and adaptive immunity. In innate immunity, the body utilizes a general responses to initially combat pathogens. In the adaptive immune response, T and B lymphocytes fight the pathogens. Antibodies are proteins made by B lymphocytes that help combat bacteria and toxins in the body. They come in five different classes; IgM, IgD, IgG, IgE, and IgA. Each class is determined by its structure, which in turn facilitates its function. However, often functionality may twist into dysfunctionality, which in the human body can cause damage, termed immunopathology. There are three types of antibody related immunopathologies; type I, type II, and type III. These antibody related diseases range from simple allergy to rheumatoid arthritis. The following is an overview of their function and dysfunction.
46
Casutt-Meyer, Salome. "Capnocytophaga canimorsus : interaction with the innate immune system /." Basel : [s.n.], 2009. http://edoc.unibas.ch/diss/DissB_8882.
Full text
47
Bi, Ran. "Immune-inspired fault diagnosis for a robotic system." Thesis, University of York, 2012. http://etheses.whiterose.ac.uk/2208/.
Full textAbstract:
To achieve fully autonomous systems, fault tolerance is often employed. Fault tolerance is the ability to continue operation in the presence of faults. Fault diagnosis is an essential component of fault tolerance, especially for autonomous robotics. It is the process of determining as much information as possible about the fault, especially the origin of the fault. However, a real time fault diagnosis for resource limited robotic systems has proposed a new set of challenges, such as its complexity and efficiency, which traditional methods will find difficult to meet. This has led the work to seek inspiration from the immune system, where an effective and efficient fault diagnosis solution has been provided for thousands of years. This thesis presents a novel immune-inspired on-line fault diagnosis algorithm for robotic systems and includes the first application of that Artificial Immune System to robot fault diagnosis.
48
Bernstein, Ralph Michael. "The molecular origins of the recombining immune system." Diss., The University of Arizona, 1996. http://hdl.handle.net/10150/187475.
Full textAbstract:
This dissertation examines the molecular origins of the recombining immune system. Two strategies were adopted involving the examination of the immune system of the most ancient extant organism possessing the vertebrate type immune response, the Carcharhine shark. First, the structural components of a primordial immunoglobulin (Ig) were examined on a molecular level. This revealed a new class of Ig termed IgW. Although IgW is the largest Ig yet described, with 7 bona fide Ig domains, it maintains the canonical residues typified by heavy chain V and C-regions. Because of these canonical residues, IgW is thought to both dimerise with light chains and associate with antigen as a typical heavy chain. IgW also possesses V-regions which are more similar to its own C-regions than any Ig yet described. In phylogenetic tree analysis, the IgW molecule is continually found to be the "root" of the Ig V and C-region trees constructed from the known V and C-region genes. This, and IgW's V and C-region similarities support the contention that IgW is the most ancient Ig yet cloned, possibly being most closely related to the primordiallg gene. The second strategy adopted was the examination of the shark's V(O)J rearrangement machinery. The recombinase activating gene I (RAG I) is responsible for creating diversity in all extant gnathastomes, which is the hallmark of the recombining immune system. The shark RAG I was found to be extremely homologous to the known vertebrate RAG I genes, both at the nucleotide and amino acid levels (∼64 % identical at both levels). Homology domains identified by the comparison of the vertebrate RAG I's and the shark RAG I prompted sequence comparison analyses which suggested similarity of the RAG I and II genes to the integrase family and the integration host factor genes, respectively, of the bacterial site specific recombination system. This was used in conjunction with several shark VH "hairpin" detecting rearrangement intermediate experiments to propose a new and more complete model of V(D)J recombination.
49
McEwan, Chris. "Representation and decision making in the immune system." Thesis, Edinburgh Napier University, 2010. http://researchrepository.napier.ac.uk/Output/4157.
Full textAbstract:
The immune system has long been attributed cognitive capacities such as "recognition" of pathogenic agents; "memory" of previous infections; "regulation" of a cavalry of detector and effector cells; and "adaptation" to a changing environment and evolving threats. Ostensibly, in preventing disease the immune system must be capable of discriminating states of pathology in the organism; identifying causal agents or ``pathogens''; and correctly deploying lethal effector mechanisms. What is more, these behaviours must be learnt insomuch as the paternal genes cannot encode the pathogenic environment of the child. Insights into the mechanisms underlying these phenomena are of interest, not only to immunologists, but to computer scientists pushing the envelope of machine autonomy. This thesis approaches these phenomena from the perspective that immunological processes are inherently inferential processes. By considering the immune system as a statistical decision maker, we attempt to build a bridge between the traditionally distinct fields of biological modelling and statistical modelling. Through a mixture of novel theoretical and empirical analysis we assert the efficacy of competitive exclusion as a general principle that benefits both. For the immunologist, the statistical modelling perspective allows us to better determine that which is phenomenologically sufficient from the mass of observational data, providing quantitative insight that may offer relief from existing dichotomies. For the computer scientist, the biological modelling perspective results in a theoretically transparent and empirically effective numerical method that is able to finesse the trade-off between myopic greediness and intractability in domains such as sparse approximation, continuous learning and boosting weak heuristics. Together, we offer this as a modern reformulation of the interface between computer science and immunology, established in the seminal work of Perelson and collaborators, over 20 years ago.
50
Yaqoob, Parveen. "The effects of fatty acids on the composition and functions of lymphocytes." Thesis, University of Oxford, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.359567.
Full text