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1

Kajbaf, Mohammad Javad. "Immunology of trachoma". Thesis, University of Southampton, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.236213.

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2

Veenstra, van Nieuwenhoven Angélique L. "Immunology of pregnancy". [S.l. : [Groningen : s.n.] ; University of Groningen] [Host], 2009. http://irs.ub.rug.nl/ppn/.

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3

Mangano, Valentina D. "Dissecting the complexity of human susceptibility to Plasmodium falciparum malaria : genetic approaches /". Doctoral thesis, Stockholm : Wenner-Gren Institute for Experimental Biology, Stockholm University, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-8310.

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4

Hutchings, Nicholas James. "Proteome analysis in immunology". Thesis, University of Oxford, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.393404.

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5

Venkatesan, Pradhib. "Immunology of murine giardiasis". Thesis, Nottingham Trent University, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.281702.

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6

Humphreys, Kenneth Andrew. "Intestinal immunology in man". Thesis, University of Edinburgh, 2001. http://hdl.handle.net/1842/22330.

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Loss of IgG to the gut in patients with inflammatory bowel disease (IBD) can arise from plasma or by local production from cells in the lamina propria. The source of IgG in WGLF was shown to be predominantly plasma since the relative coefficient of excretion for IgG in WGLF was similar to albumin for all colonic IBD patients with a range of disease activity. As albumin is much mores susceptible to proteolysis than are immunoglobulins, the study was restricted to patients with colonic disease and without extremes of WGLF protease activity. It has been assumed that protein loss occurs from the site diagnosed as diseased by clinical assessment. To confirm that plasma leakage is the major source of WGLF IgG in patients with colonic IBD, loss of another plasma protein, complement C3, was investigated. A competitive ELISA was developed to measure C3 in WGLF. This requires binding of a single antibody which enables detection of both immune complexes and free C3. WGLF C3 was raised in patients with active IBD. This loss mirrored that of IgG and albumin, showing no diagnostic specificity. In patients with ulcerative colitis, the relative loss of C3 was similar to that of albumin. In contrast, patients with colonic Crohn's disease (CD) show twofold loss of C3 relative to albumin, indicating that mucosal production was a major contributor to WGLF C3. As patients with inactive CD had slightly raised WGLF C3, this may indicate early clinical relapse. The relationship between WGLF C3 and relapse of CD was investigated by follow up of 43 patients for one year after gut lavage. Of 10 who relapsed, 8 had normal WGLF C3 whereas of 15 patients who remained in steroid free remission, 8 had raised WGLF C3. There was a risk factor of 4.4 for relapse in patients with inactive CD who had normal WGLF C3. This might suggest complement deposition or a protective role of complement e.g. clearing apoptotic cells. These hypotheses could be further investigated using intestinal biopsies. This work has been supported in part form a MRC grant to exploit the potential of WGLF.
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7

Bui, Naomi Nhu. "Immunology of Tumamoc Hill". Thesis, The University of Arizona, 2014. http://hdl.handle.net/10150/319939.

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8

Tjärnlund, Anna. "Mucosal Immunity in Mycobacterial infections". Doctoral thesis, Stockholm University, Wenner-Gren Institute for Experimental Biology, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-6782.

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More than a century after the identification of the tubercle bacillus and the first attempts at vaccination, tuberculosis (TB) still remains one of the world’s most serious infectious diseases. TB, caused by the bacterium Mycobacterium tuberculosis, is typically a disease of the lung, which serves both as port of entry and as the major site of disease manifestation. The currently used vaccine, BCG, is administered parenterally and induces a systemic immune response. However, it fails to protect against pulmonary TB, thereby raising the question whether vaccination targeting the mucosal immunity in the lungs could be favourable.

The respiratory mucosal surfaces represent the first line of defence against a multitude of pathogens. Secretory IgA, in mucosal secretions has an important function by blocking entrance of pathogenic organisms and preventing infections. Additionally, a role for IgA in modulation of immune responses is currently being revealed. In this work, we investigated the relevance of mucosal IgA in protection against mycobacterial infections using mice deficient for IgA and the polymeric Ig receptor, the receptor responsible for mucosal secretions of IgA. Gene-targeted mice were more susceptible to mycobacterial infections in the respiratory tract and displayed reduced production of proinflammatory, and protective, factors such as IFN-γ and TNF-α in the lungs. The mechanisms explaining the defective proinflammatory responses in the lungs of deficient mice might involve impaired signalling through Fcα receptors, or homologous receptors, which could lead to inadequate activation of pulmonary macrophages. This could subsequently result in suboptimal induction and production of cytokines and chemokines important for attraction and migration of immune cells to the site of infection.

Induction of optimal adaptive immune responses to combat mycobacterial infections requires prompt innate immune activation. Toll-like receptors (TLRs) are vital components of the innate branch of the immune system, ensuring early recognition of invading pathogens. Using TLR-deficient mice we demonstrated an important role for TLR2, and partly TLR4, in protection against mycobacterial infection in the respiratory tract. TLR2-deficient mice failed to induce proper proinflammatory responses at the site of infection, and macrophages derived from the knockout mice displayed impaired anti-mycobacterial activity.

Experimental evidence has concluded that the immune response upon an infection can influence the outcome of succeeding infections with other pathogens. Concurrent infections might additionally interfere with responses to vaccinations and have deleterious effects. We developed an in vitro model to study the effect of a malaria infection on a successive M. tuberculosis infection. Our results demonstrate that a malaria blood-stage infection enhances the innate immune response to a subsequent M. tuberculosis infection with a Th1 prone profile. Reduced infectivity of malaria-exposed dendritic cells implies that a malaria infection could impose relative resistance to ensuing M. tuberculosis infection. However, a prolonged Th1 response may interfere with malaria parasite control.

The outcome of this work emphasizes the importance of generating effective immune responses in the local mucosal environment upon respiratory mycobacterial infections. It furthermore puts new light on the immunological interaction between parasites and mycobacteria, which could have implications for future vaccine research.

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9

Vafa, Manijeh. "Human genetic factors in relation to Plasmodium falciparum infection". Licentiate thesis, Stockholm University, Wenner-Gren Institute for Experimental Biology, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-7136.

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10

Israelsson, Elisabeth. "The role of antibody mediated parasite neutralization in protective immunity against malaria". Licentiate thesis, Stockholm University, Wenner-Gren Institute for Experimental Biology, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-7137.

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11

Sjögren, Ylva. "Early infant gut flora and neutral oligosaccharides in colostrum in relation to allergy development in children". Licentiate thesis, Stockholm University, Wenner-Gren Institute for Experimental Biology, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-7152.

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Today, atopic allergy is the most common chronic disease among children in the developed world. The increase in allergy prevalence during the past decades in these countries might be associated with lower microbial exposure. The gut flora, consisting of approximately 800 different species of bacteria, has been postulated to be important for the development of a fully functional immune system. Essentially, these bacteria are in constant contact with the gut flora associated lymphoid tissue, the largest lymphoid tissue of the human body. Following birth, the sterile gut of the newborn is immediately colonised by various bacterial species. Actually, alterations in the infant gut flora have been associated with allergy development.

Human milk is the major food in infancy and could thus influence the composition of the infant gut flora. Immunomodulatory components in human milk might differ between mothers and could therefore explain the contradictory results seen regarding breastfeeding and allergy development. Oligosaccharides, the third most abundant solid component in human milk, survive the passage through the stomach and are utilised by the gut microbiota. We analysed nine abundant neutral oligosaccharides in colostrum samples from allergic and non-allergic women and related to subsequent allergy development in their children. We found a considerable variation in the concentration of neutral oligosaccharides in colostrum, which was not to be explained by the allergic status of the women. Neither was the consumption of neutral colostrum oligosaccharides related to the allergy development in children.

Relevant bacterial species in early faecal samples were analysed, with Real-time PCR, and related to allergy development in children followed up to five years of age. Infants who harboured Lactobacilli (L.) group I (L. rhamnosus, L. paracasei, L. casei) at 1 week of age and Bifidobacterium adolescentis at 1 month of age developed allergic disease less frequently during their first five years than infants who did not harbour these bacteria at the same time (p=0.004 and p=0.008 respectively).

In conclusion, the work presented in this thesis implies the importance of a diverse gut flora early in life for the development of a fully functional immune system. However, consumption of colostrum with high amounts of neutral oligosaccharides does not protect against early allergy development.

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Ali, Magdi Mahmoud. "Immunologic aspects of the pathogenesis of human onchocerciasis". Doctoral thesis, Stockholm University, Wenner-Gren Institute for Experimental Biology, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-793.

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Onchocerciasis, or river blindness, is a parasitic disease that affects more than 20 million people globally. The induction of pathology is directly related to the presence and destruction of the microfilarial stages (mf) of this filarial nematode. The disease presents clinically with a wide spectrum of dermal and ocular manifestations, the basis of the variation is believed to involve the immune system. The clinical presentations of infected hosts relate to the intensity of the reactions against the parasite. Anti-microfilarial drugs are also thought to somehow involve the immune system in their pharmacological action. In this study we have investigated some of the factors that might contribute to the pathogenesis, with the aim of gaining a better understanding of the role of immune response in these host inflammatory reactions to Onchocerca volvulus parasite. In the first study we have highlighted the clinically most severe form of dermal onchocerciasis, known as reactive onchocercal dermatitis (ROD), one that is often ignored and has not been properly identified. This form has special characteristics and important biological information that could greatly assist the general understanding of the disease as a whole. Amongst the three major foci of the disease in the study country, Sudan, the prevalence of ROD was found to be associated with different environmental and epidemiological characteristics; strikingly higher in the hypo-endemic areas. Including ROD cases in the prevalence will upgrade the level of endemicity of a locality, and often bring patients much in need of treatment into mass treatment programs that currently only treat localities with medium to high levels of endemicity. In the following research studies, we tried to address the immunological characteristics of the clinically different onchocerciasis patients. Then we also investigated the role of genetic polymorphism in the gene encoding receptor that links innate and adaptive immunity, namely, FcγRIIa.

Patients with either of two major forms of the clinical spectrum-mild and severe dermatopathology were studied by assaying the antigen-driven proliferation of peripheral blood mononuclear cells and the ability of patients’ serum antibodies to promote cytoadherence activity to mf in vitro. Immune responses of those with severe skin disease were found to be stronger compared with the mild dermatopathology group. Mectizan® treatment was followed by an increase in immune responsiveness in those with initially poor responses. Thus the degree of dermatopathology is related to the host’s immune response against mf and immunocompetence may be necessary for Mectizan® to clear the infection efficiently.

The infection has also been associated with increased levels of circulating immune complexes (CIC) containing parasite antigens and a cytokine response that involves both pro-and anti-inflammatory cytokines. Our fourth paper investigated the effect of IC from the O. volvulus infected patients on the production of pro-and anti-inflammatory cytokines. CIC were increased in all patients studied. The precipitate from plasma treated with polyethylene glycol (PEG) were added to peripheral blood mononuclear cell (PBMC) cultures, and the levels of IL-10, tumor necrosis factor TNF-α, IL-1β and their endogenous antagonists soluble TNF-Rp75 and IL-1-receptor antagonist (IL-1ra) were measured. A significant induction of all cytokines measured occurred in the onchocerciasis patients compared to healthy controls. However, the IL-1ra level was suppressed. The suppression of the production of IL-1ra suggests that the IC containing antigens may have a selectively suppressive effect on the production of this anti-inflammatory cytokine; thus implicating its possible role in counteracting inflammatory responses associated with the disease, and suggesting a potential therapeutic significance.

FcgRIIa receptors are involved in many important biological responses, and considered as important mediators of inflammation. A polymorphism in the gene encoding this receptor, that is either arginine (R) or histidine (H) at position 131, affects the binding to the different IgG subclasses. We therefore hypothesized that this polymorphism might be one of the underlying mechanisms to the varied clinical presentations seen in this disease. FcgRIIa genotyping was carried out by gene specific polymerase chain reaction (PCR) and allele-specific restriction enzyme digestion of DNA from clinically characterized patients. The genotype R/R frequencies were found to be significantly higher among patients with the severe form of the disease (including ROD), and it was particularly associated with one tribe (Masaleet) compared to Fulani. Moreover, the H allele was found to be associated with lower risk of developing the severe form. As no significant difference was seen between onchocerciasis cases and controls, the study also implies that this polymorphism influences protection from developing the severe form rather than being related to protection from the infection.

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13

Rahman, Muhammad Jubayer. "Diagnostic biomarkers and improved vaccination against mycobacterial infection". Licentiate thesis, Stockholm University, Wenner-Gren Institute for Experimental Biology, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-8238.

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Tuberculosis (TB) remains one of the world’s most serious infectious diseases. It is estimated that a third of the world’s population is latently infected and 8 million new cases are recorded each year. Although BCG vaccination triggers protective immune responses in the neonates, it confers protection against only certain forms of childhood TB. Protection mediated by BCG, against pulmonary TB, is controversial as reported with variable efficacy ranging from 0-80%. In addition to the problems associated with the BCG vaccine, diagnosis of TB cannot be performed readily with the available tools. At present, an effective control of TB is highly dependent on the development of a new TB-vaccine as well as proper identification and treatment of individuals with active disease. Therefore, we particularly focused on identification of biomarker (s) of infection and the development of better vaccines, with special emphasis on the immune responses in the respiratory tract.

In the first study, we aimed to identify immune biomarker (s) of infection for better diagnosis of TB. Mice were infected with BCG administered i.n. or i.v., and the bacterial burden in the lungs, spleen and liver was examined. We measured IL-12, IFN-γ, TNF, soluble TNF receptors (sTNFR) and mycobacteria-specific antibodies in the broncho-alveolar lavage (BAL) and in serum in order to find immune correlates of infection. Results showed that sTNFR and mycobacteria-specific antibodies in BAL, but not in serum, might be useful in distinguishing active from latent infection or exposure to mycobacterial antigens.

In the second study, we investigated whether we could improve the currently used BCG vaccine. For this purpose, we tested a combination of neonatal vaccination protocol using BCG and posterior boosting with the protein heparin-binding hemagglutinin adhesion (HBHA). It has been described that immunization with native (n) HBHA but not recombinant (r) HBHA conferred protection against M. tuberculosis challenge in mice.

This protection was comparable to that afforded by the BCG vaccine. In order to improve the protective efficacy of the nHBHA vaccine we followed heterologous prime-boost strategy, comprising BCG vaccination at the neonatal age, followed by nHBHA boosting at the infant and adult ages. We also examined whether the rHBHA protein could boost BCG-mediated protective immunity. Cellular immune responses and protection as measured by control of bacterial growth in the lungs of the treated animals were followed. Our results showed an improved effect of BCG-priming on HBHA-immunization. The BCG/HBHA immunization protocol was more effective in induction of HBHA-specific immune responses, as well as in protection than when the animals received only BCG or HBHA alone. Importantly, our study revealed that nHBHA does not require co-administration with adjuvant provided that mice were primed with live BCG before boosting.

Finally, we hypothesized that in utero sensitization of the fetal immune system with nHBHA may improve nHBHA-specific immune responses after birth. The pregnant mother was immunized with nHBHA 1 week before delivery. After birth, the offspring received two doses (week 1 and week 4) of nHBHA formulated with cholera toxin. We examined HBHA-specific recall responses and protection after challenge with a high dose of BCG. We found that immune responses were improved by priming the pregnant mother, and that this also provided better protection than when the offspring received only BCG or HBHA neonatal vaccinations.

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14

Sundström, Yvonne. "Phenotypic and functional studies of NK cells in neonates and during early childhood". Doctoral thesis, Stockholms universitet, Wenner-Grens institut för experimentell biologi, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-8258.

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During infancy, before adaptive immunity has matured, innate immunity is thought to be relatively more important. Human natural killer (NK) cells are innate immune cells involved in the control of virus-infected cells and can influence adaptive immunity mainly through cytokine production. This thesis aimed at investigating function and phenotype of NK cells in children from birth and during early childhood and to see if these features are altered in children that develop early allergy, in children latently infected by herpes viruses or born by preeclamptic mothers. Our results suggest that NK-cell populations are dynamic during the first years of life and start to resemble the phenotype of adults after five years of age. Early alterations in the NK-cell populations could lead to insufficient Th1 priming, with an increased risk to develop allergic disease. Early infection by common herpes viruses can influence NK-cell function and might be one important factor involved in early maturation processes of adaptive immunity. The altered NK-cell function and cytokine levels, noticed in CB from pathological pregnancies, suggest that NK cells could be influenced already in utero. These early alterations of innate immunity may affect the development of the child’s immune system, sometimes with beneficial outcome but could in some cases promote pathology.
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Walldén, (Fredriksson) Jenny. "Studies of immunological risk factors in type 1 diabetes". Doctoral thesis, Linköpings universitet, Pediatrik, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-12441.

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Background: Type 1 diabetes (T1D) is a chronic, autoimmune disease caused by a T cell mediated destruction of ß-cells in pancreas. The development of T1D is determined by a combination of genetic susceptibility genes and environmental factors involved in the pathogenesis of T1D. This thesis aimed to investigate diverse environmental and immunological risk factors associated with the development of T1D. This was accomplished by comparing autoantibody development, T cell responses and the function of CD4+CD25+ regulatory T cells between healthy children, children at risk of T1D and T1D patients. Results: Induction of autoantibodies in as young children as one year old, was associated with previously identified environmental risk factors of T1D, such as maternal gastroenteritis during pregnancy and early introduction of cow’s milk. We did not see any general increase in the activity of peripheral blood TH subtypes in children with HLA class II risk haplotypes associated with T1D, nor were HLA class II risk haplotypes associated with any aberrant cytokine production in response to antigenic stimulation of peripheral blood mononuclear cells. However children with a HLA class II protective haplotype showed an increased production of IFN-γ in response to enteroviral stimulation. CTLA-4 polymorphisms connected with a risk of autoimmune disease were associated with enhanced production of IFN-γ. Healthy children with ß-cell autoantibodies had a lower expression level of GATA-3 compared to health children with HLA risk genotype or children without risk. Instead, children with manifest T1D showed lower expression levels of T-bet, IL-12Rß1 and IL-4Rα. Both T1D and healthy children showed the same expression of the regulatory markers Foxp3, CTLA-4 and ICOS in peripheral blood mononuclear cells, and the amount of CD4+CD25+ T cells did neither reveal any differences. The regulatory T cells seemed also to be functional in children with T1D, since increased proliferation after depletion of CD4+CD25high cells from PBMC was demonstrated in T1D as well as in healthy children.However, T1D children did have more intracellular CTLA-4 per CD4+CD25high T cell, increased levels of serum C-reactive protein and higher spontaneous expression of IFN-α in CD25depleted PBMC, all which are signs of activation of the immune system. This suggests a normal or enhanced functional activity of regulatory T cells in T1D at diagnosis. Conclusions: Our findings emphasize that environmental risk factors do have a role in the development of ß-cell autoimmunity. Our results do not support a systemic activation of the immune system in pre-diabetes or T1D, but instead a possible up-regulation of regulatory mechanisms seems to occur after diagnosis of T1D, which probably tries to dampen the autoimmune reaction taking place.
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16

Amoudruz, Petra. "Maternal immune characteristics and innate immune responses in the child in relation to allergic disease". Doctoral thesis, Stockholms universitet, Wenner-Grens institut, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-7818.

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The mechanistic factors responsible for the increase in allergic diseases are still not fully understood, but a reduced microbial stimulation seems to be one of the key issues. Research is now aiming at investigating the relationship between the innate immune system, involving the toll-like receptors, and allergy development. Further, the maternal influence on the child, possibly through in utero effects, but also through the breast milk, has shown to be of great importance. This thesis aimed at understanding how the maternal immune system is influenced by early exposures and allergic disease, but also to investigate the consequences of the maternal phenotype on the innate immune system of the developing child. The Th1/Th2 cytokine pattern in allergic diseases has been extensively studied. Here we were interested in comparing the innate cytokines in allergic and non-allergic women, and to see if the allergic status was influencing the effect of pregnancy differently. We demonstrate that IL-1β, IL-6, IL-10 and IL-12 production in cells from adult women are not influenced by allergic status, neither during pregnancy nor 2 years after. However, pregnancy had an apparent effect on cytokine levels, regardless of allergic status. Also, total IgE levels in allergic women were significantly lower 2 years after pregnancy in comparison with the levels during pregnancy, pointing to the fact that pregnancy indeed has an immunomodulatory role. We further wanted to investigate the immune system of mothers who had migrated to Sweden in comparison with indigenous mothers. The reason for our interest here was that children born from immigrated mothers have shown to have an increased risk of developing diseases such as allergy and Crohn’s disease. The results showed that immigrants from a developing country had significantly higher levels of breast milk IL-6, IL-8 and TGF-β1. Further, regardless of maternal country of birth, a larger number of previous pregnancies was associated with down-regulation of several substances, statistically significant for soluble CD14 and IL-8. The results suggest that maternal country of birth may indeed influence adult immune characteristics, potentially relevant to disease risk in offspring. The influence of allergic status of the mother on the expression of CD14, TLR2 and TLR4 was further investigated in monocytes from mothers and their newborn babies upon microbial stimulation. We could not find any differences in monocytic TLR levels between the groups. No significant differences regarding cytokine levels between allergic and non-allergic mothers in response to stimuli were found either. However, the cytokine and chemokine release triggered by TLR2 stimulation in CB revealed that CBMC from children with maternal allergic disease released significantly less IL-6, and a trend towards less IL-8. As we could not find differences in TLR levels attributed to maternal allergy, but an impaired IL-6 response, we turned our focus on an intracellular event taking place after TLR ligation. The results confirmed our results of decreased IL-6 levels in CB from children to allergic mothers. At 2 years of age, the children of allergic mothers still displayed a diminished IL-6 response. Additionally, they also had a decreased activity of p38 MAPK. p38 has an important role in driving Th1 responses, suggesting that the p38 pathway could be one of the responsible mechanisms behind the impaired responses correlated to allergic heredity found in CB as well as at 2 years of age. Infancy is a crucial time period for the developing immune system. Further, the relative composition of the two major monocytic subsets CD14++CD16- and CD14+CD16+ is altered in some allergic diseases. TLR levels are different in the two subsets, proposing a possible link to the reduced responding capacity of monocytes from children with allergic heredity. We followed up our earlier studies of children at birth and at 2 years of age by looking at 5 year old children. There were no differences regarding monocytic subsets, nor in TLR levels in unstimulated cells. However, when stimulating the cells with PGN, both monocytic subsets in allergic subjects were less capable of upregulating TLR2 compared to the age-matched controls. Taken together, the work in this thesis suggests that the maternal immune system is affected by the process of pregnancy and childhood exposures. It further suggests that maternal allergy affects the young child, in terms of impaired responses to microbial stimuli, which later in infancy correlates with allergic disease in the child. These impaired innate responses could lead to a diminished Th1 response, or alternatively to a deficiency in regulatory mechanisms, and thereby cause allergic disease.
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Sohlberg, Ebba. "Innate immune responses in cord blood,and the influence of pathological pregnancy". Licentiate thesis, Stockholms universitet, Avdelningen för immunologi, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-54575.

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18

Balogun, Halima Aramide. "Immunological characteristics of a C-terminal fragment of the Plasmodium falciparum blood-stage antigen Pf332". Licentiate thesis, Stockholms universitet, Wenner-Grens institut, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-7143.

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Abstract (sommario):
Till date, there are no effective control strategies against the deadly disease of malaria, and millions of children across Africa, Oceania, Asia, and Latin America are at the mercy of this long term enemy of man every second that passes by. Other control measures combined with vaccination might help improve control strategy against malaria, but the development of vaccines face various challenges as well, due to the complexity of the parasites’ life cycle and other host factors. The asexual blood stage antigen Pf332 of Plasmodium falciparum, is expressed during the trophozoite stage, and transported from the parasitophorous membrane to the outer erythrocyte membrane during schizogony. Previous studies have suggested this antigen as a potential vaccine candidate, because Pf332-reactive human monoclonal antibody (mAb 33G2) inhibits parasite growth and cytoadherence in vitro. Elucidating and understanding the immunological capabilities of antigen Pf332, as a vaccine candidate was the aim of the studies presented in this thesis. In our first study we identified and characterized the immunogenicity of a non-repeat fragment of antigen Pf332, termed Pf332-C231, a 231 amino acids long fragment corresponding to 13 percent of the total protein. Various analyses carried out with this fragment reveal that recombinant C231 was immunogenic in rabbits. In addition, anti- C231 antibodies have in vitro inhibitory capabilities. In immunoflourescence and immunoblot assays, rabbit anti-C231 antibodies were able to recognize the native protein. In the other study, we examined the distribution of antibodies regarding recombinant C231 and crude P. falciparum extract in a malaria endemic area of Senegal. IgG antibody reactivity with crude P. falciparum antigen was detected in the sera of all the  donors while many of the children lacked or had low levels of such antibodies against C231. The distribution of the anti-C231 antibodies in the different IgG subclasses differed from that shown by crude P. falciparum antigen. The crude P. falciparum antigen gives a higher IgG3 response than IgG2 for all age-groups, while C231 gave similar levels of IgG2 and IgG3. Correlation studies showed that the levels of anti-C231antibodies were associated with protection from clinical malaria, but this only reached significance with IgE. These findings further emphasize the inclusion of antigen Pf332 as a subunit vaccine candidate against P. falciparum malaria.
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19

Awah, Nancy. "Malarial anaemia : the potential involvement of Plasmodium falciparum rhoptry proteins". Licentiate thesis, Stockholms universitet, Wenner-Grens institut, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-8460.

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Abstract (sommario):
Malaria remains a challenging health problem in malaria endemic regions. Infection with malaria invariably leads to anaemia. The groups at risk of developing malarial anaemia include children below the age of five years and pregnant women, especially primigravidae. Several factors have been suggested to be responsible for its aetiology, including increased destruction of infected and normal red blood cells together with bone marrow suppression. However, until recently, the molecular mechanisms involved have remained elusive. The aim of the work presented herein was to investigate the mechanisms responsible for the destruction of normal red blood cells in anaemia, and more specifically to define the role of the ring surface protein (RSP/RAP) -2 and other members of the low molecular weight rhoptry associated protein (RAP) complex, RAP-1 and -3. In the first study we showed that antibodies to the RAP complex could mediate the destruction of RSP-2 tagged erythroid cells by phagocytosis or by complement activation and then lysis. In addition, antibodies to RAP-1 and RAP-2 could induce the death of RSP-2/RAP-2 tagged erythroblasts. We further investigated the frequency and functionality of naturally occurring RSP-2/RAP-2 antibodies in the sera of anaemic and non-anaemic Cameroonian children. We found that all sera investigated contained RSP-2/RAP-2 reactive antibodies by both immunoflorescence and flow cytometry. The anaemic group of children had significantly higher levels of antibodies of the IgG isotype than the non-anaemic individuals, while the levels of IgM were similar in both groups. With respect to IgG subclasses, low levels of IgG1 and -3 antibodies were detected. Higher levels of IgG3 were seen in the non-anaemic individuals as compared to anaemic subjects. With regards to antibody functionality, the non-anaemic individuals recognised a greater proportion of RSP-2/RAP-2 tagged erythrocytes and activated complement to a greater extent than the anaemic individuals. From our findings, we can conclude that antibodies to the RAP complex are potentially involved in erythroid cell destruction during malaria which may result in anaemia, and that high levels of such antibodies may be detrimental to the host.
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20

Newsom-Davis, Thomas Edmund. "Fas Ligand and Tumour Immunology". Thesis, Imperial College London, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.486884.

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Fas ligand (FasL) is a transmembrane protein which induces apoptosis in cells expressing its receptor, Fas. The FasL/Fas pathway is one ofthe major mediators of cell death in the immune system but more recently an inflammatory role has been suggested. This thesis investigated the finding that when injected into mice, FasL-expressing (FasL+) tumours recruit a massive polymorphonuclear neutrophil (PMN) infiltration and are then rejected, which is followed by the development of antibody mediated tumour immunity. . In this work, eight IgM and one IgG2a monoclonal antibodies (mAbs) were produced from mice vaccinated with FasL+ murine melanoma. They recognised various syngeneic and allogeneic murine tumours cell lines. One mAb, TMIO, also recognised a range of human tumours cell lines but not untransformed cells. The epitopes of all the mAbs were carbohydrates expressed on proteins and/or lipids. The epitope of TMIO were high-mannose clusters on N-linked glycoproteins whilst another antibody, KM5.2, was recognising the glycolipid GM4. Both are novel tumour antigens. The IgG2a mAb had in vivp anti-tumour activity, protecting mice against the development ofboth cutaneous and metatstatic melanoma through antibody dependent cellular cytotoxicity. T~e mechanism behind the rejection and immunity to FasL+ tumours was studied using human cells. FasL promoted the production of chemokines by PMNs. PMNs, but not FasL, induced maturation of dendritic cells with a corresponding increase in T cell proliferation. FasL inhibited the generation of the THI subset ofCD4+ T cells, whereas PMNs promoted THI polansation and increased 1NFa and IL-22 production. -- , A model is proposed in which PMNs attracted to the tumour site promote rejection of FasL+ tumours by creating an inflammatory environment whilst recruiting and activating effector cells. They then induce antibody-mediated tumour immunity by facilitating the T cell help required. PMNs therefore act as a bridge between the innate and adaptive immune responses.
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21

Howes, Moira Ann. "Immunology and the indiscrete self". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape9/PQDD_0008/NQ42530.pdf.

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22

Sheu, Eric G. "Immunology of T cell vaccines". Thesis, University of Oxford, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.288552.

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23

Figueredo, Grazziela P. "Translating simulation approaches for immunology". Thesis, University of Nottingham, 2012. http://eprints.nottingham.ac.uk/12905/.

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Abstract (sommario):
This thesis presents a novel set of guidelines to convert between simulation modelling approaches, namely, Ordinary differential Equations (ODEs), System Dynamics (SD) and Agent-based Modelling and Simulation (ABMS). In our literature review we identify a gap in establishing translation techniques between these approaches. We therefore focus our research in developing these techniques and assessing the impact of these conversions in the simulation outcomes. In particular, our interest lies in investigating our techniques applied to simulation problems for the immune system, as we wish to aid immunologists with the choice of the most appropriate approach for a certain problem. The aims of this thesis are therefore defined as: (1) with no explicit guidelines available from the literature, we want to develop, test and validate our own set of guidelines for converting between approaches: from ODE models to SD, from SD to ABMS and from ABMS to SD; and (2) we seek to discuss the merits of SD and ABMS for Immunology to assist researchers with the choice between both approaches. The assessment of the effectiveness of the conversion guidelines is achieved by using a case study approach involving six cases of established mathematical models describing immunological phenomena. These case studies are chosen by considering aspects such as the behaviour of the entities of the model (whether they are static or interact with other entities and whether they have spatial representation or not), the type of hypothesis to be tested, the empirical embeddedness of real data, population sizes, number of elements involved and the modelling effort. In order to conduct our conversion for the case studies, we first convert their original ODE model into an SD model, and then perform the translation from SD to ABMS. For the last three case studies, we also test the conversion guidelines from ABMS to SD. Evidence from the experiments reveal that for all cases it was possible to obtain equivalent approaches by using the conversion guidelines developed. However, outcome differences occur given the intrinsic characteristics of each simulation modelling paradigm. By observing these differences we could conclude that (1) SD is incapable of reflecting exactly the same variability as that obtained from the agent-based simulation, as it is a deterministic approach; (2) SD variables change continuously in time and therefore population numbers over time might be different from those obtained by the agent-based simulation; (3) as the number of different agents and behaviours increase, the corresponding SD becomes very intricate and difficult to develop and understand; (4) there are cases where it is preferable not to convert from ABMS to SD, as the agent-based model is easier to conceptualise and implement; (5) For other circumstances, ABMS outcomes are the same as those produced by the ODEs and SD, with the disadvantage to be more resource consuming in terms of computational memory and processing capacity; and (6) For some cases SD is less informative than ABMS, as it does not produce multiple scenarios or variations over the course of more than one run within the same parameters.
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24

Zhao, Yuan. "Immunology of granulomatosis with polyangiitis". Thesis, King's College London (University of London), 2013. https://kclpure.kcl.ac.uk/portal/en/theses/immunology-of-granulomatosis-with-polyangiitis(91230752-735f-41ea-8695-f26f8b2e5c97).html.

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Abstract (sommario):
Granulomatosis with polyangiitis (GPA, formerly known as Wegener’s granulomatosis) is a rare and sometimes fatal systemic autoimmune disease. Anti-neutrophil cytoplasmic antibodies (ANCAs) specific for proteinase 3 (PR3) are associated with GPA. However, the pathogenesis of GPA is not yet clear. Our aim was to investigate the local autoimmune response, circulating immune modulatory cells and cells expressing the immune suppressor molecules programmed death 1 (PD-1) and its ligands in GPA. In mucosa from GPA patients, activated B cells were observed located alongside PR3 expressing cells and B cell survival factors BAFF and APRIL, which was produced by the granulomas and giant cells. B cells were proliferating and persistent in biopsies. However no evidence of B cell clones from the mucosal biopsies circulating in peripheral blood was observed in GPA. An increased frequency of circulating TFH cells and a reduced frequency of Treg cells was observed in peripheral blood from GPA patients on conventional therapies compared to healthy controls. No such difference was found in GPA patients treated with rituximab. The frequency of circulating TFH and Treg cells was found to be inversely correlated in human peripheral blood. No difference in the relative quantity of mRNA encoding PD-1 in lymphocytes and monocytes was found in GPA patients compared with healthy controls. Lower percentage of CD14+ monocytes expressing PD-1 was observed in GPA patients. Lower relative quantity of mRNA encoding PD-1 ligands PD-L1 and PD-L2 in T cells and monocytes was observed in GPA patients. In conclusion, data in this thesis identifies activated B cells alongside auto-antigens and B cell survival factors in the mucosa in GPA. A negative correlation between TFH and Treg cells is observed that implies the balance between T cell subsets and its B cell dependence are associated with disease activity in GPA. The deficiency of PD-L1 and PD-L2 mRNA in lymphocytes and monocytes may contribute to the pathogenesis of GPA.
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25

Thompson, Fiona Mary. "Malaria immunology and vaccine development". Thesis, University of Southampton, 2008. https://eprints.soton.ac.uk/67626/.

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This thesis describes work undertaken by the author at the University of Oxford. It begins by providing an introduction to malaria infection and pathophysiology, and a review of the latest attempts to produce an effective malaria vaccine. It goes on to describe the rationale behind the vaccines developed by the University of Oxford and others. A brief introduction to the process of planning and carrying out clinical trials of vaccines is then provided, and is followed by chapters describing two clinical trials, designed to test the safety, immunogenicity and then efficacy of candidate malaria vaccines. These trials were performed in Oxford, to examine two different vaccination approaches. The first intended to broaden the specificity of the vaccine induced immune response, by providing multiple antigens in one vaccine, aiming thereby to improve protection from malaria infection. The second regimen used a combination vaccine intending to induce both humoral and cellular immunity simultaneously, thereby providing enhanced efficacy against malaria infection. Neither approach was sufficient to provide protection from infection in the challenge studies described; however, some impact on the disease was detected in the second study. This is examined in detail. The laboratory work described studies background immune responses (both cellular and humoral) to vaccine antigens in a malaria exposed population, intended to support the inclusion of these antigens in the multi-antigen vaccine. The remaining chapters describe work in parasite life cycle modelling, undertaken to aid interpretation of results of these clinical trials, and finally an examination of the clinical course of malaria in the control volunteers who have taken part in the many challenge studies conducted in Oxford.
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26

Parney, Ian Frederick. "Human glioma immunology and immunogene therapy". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape8/PQDD_0003/NQ39580.pdf.

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27

Klingström, Jonas. "Hantaviruses : animal models, immunology and pathogenesis /". Stockholm, 2004. http://diss.kib.ki.se/2004/91-7140-071-0/.

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28

Rodgers, Jackie Michele. "The immunology of hydrocephalus shunt infections". Thesis, University College London (University of London), 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.246215.

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29

Chlon, Leon. "Machine learning methods for cancer immunology". Thesis, University of Cambridge, 2017. https://www.repository.cam.ac.uk/handle/1810/268068.

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Abstract (sommario):
Tumours are highly heterogeneous collections of tissues characterised by a repertoire of heavily mutated and rapidly proliferating cells. Evading immune destruction is a fundamental hallmark of cancer, and elucidating the contextual basis of tumour-infiltrating leukocytes is pivotal for improving immunotherapy initiatives. However, progress in this domain is hindered by an incomplete characterisation of the regulatory mechanisms involved in cancer immunity. Addressing this challenge, this thesis is formulated around a fundamental line of inquiry: how do we quantitatively describe the immune system with respect to tumour heterogeneity? Describing the molecular interactions between cancer cells and the immune system is a fundamental goal of cancer immunology. The first part of this thesis describes a three-stage association study to address this challenge in pancreatic ductal adenocarcinoma (PDAC). Firstly, network-based approaches are used to characterise PDAC on the basis of transcription factor regulators of an oncogenic KRAS signature. Next, gene expression tools are used to resolve the leukocyte subset mixing proportions, stromal contamination, immune checkpoint expression and immune pathway dysregulation from the data. Finally, partial correlations are used to characterise immune features in terms of KRAS master regulator activity. The results are compared across two independent cohorts for consistency. Moving beyond associations, the second part of the dissertation introduces a causal modelling approach to infer directed interactions between signaling pathway activity and immune agency. This is achieved by anchoring the analysis on somatic genomic changes. In particular, copy number profiles, transcriptomic data, image data and a protein-protein interaction network are integrated using graphical modelling approaches to infer directed relationships. Generated models are compared between independent cohorts and orthogonal datasets to evaluate consistency. Finally, proposed mechanisms are cross-referenced against literature examples to test for legitimacy. In summary, this dissertation provides methodological contributions, at the levels of associative and causal inference, for inferring the contextual basis for tumour-specific immune agency.
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30

Rezvan, Hossein. "Studies on immunology of Leishmania mexicana". Thesis, Nottingham Trent University, 2007. http://irep.ntu.ac.uk/id/eprint/181/.

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Abstract (sommario):
Leishmaniasis is a worldwide disease prevalent in many tropical and sub tropical countries. Treatment of Leishmaniasis by chemotherapy is not wholly effective and is usually accompanied by unpleasant side effects. The development of an effective and inexpensive vaccine represents a practical way to control the disease, however at present no safe and effective vaccine is available. In the first part of the present study, the immunity induced by four different L. mexicana potential vaccines, including killed leishmania vaccine, Soluble L. mexicana Antigen (SLA), L. mexicana gp63 cDNA and CT26 tumour cells transfected with L. mexicana gp63, were compared. It was shown that DNA immunisation using L. mexicana gp63 generated the highest immunity to the parasite among the four tested vaccines where the killed leishmania vaccine and L. mexicana gp63 transfected CT26 tumour cells did not generate significant immunity. The efficacy of DNA immunisation by intramuscular injection or using gene gun, in generating immunity to leishmania was compared. Gene gun immunisation induced more immunity to the parasite and high levels of Th1 immune response, which were detected, one week after immunisation through determination of the IgG2a levels in blood serum. Gene gun immunisation also induced long-lasting CTL activity, which was detectable before and during the course of infection for up to 6 months. Immunogenicity of MHC class I restricted peptides derived from L. mexicana gp63 have been investigated. Using 'SYFPEITHI' software, four peptides with high affinity to human HLA-A2 and four peptides with high affinity to mouse H2-Ld were predicted, synthesized and tested in HHD II and BALB/c mice respectively. Only three of the peptides predicted with high affinity to HLA-A2 were immunogenic but only two of them were likely to be naturally processed, however, none were protective in HHD II mice against leishmania infection. Purification and application of OX40L, a ligand for T-cell co-stimulatory receptor, was investigated in L. mexicana BALB/c model. In addition to purification by protein A sepharose, the murine OX40L-IgG fusion protein produced by B9B8E2 cells (cells transfected with OX40L and IgG) was successfully purified by two novel resins, MBI & MEP. The biological activity of the OX40L-IgG purified by MBI resin was significantly higher than that of MEP or protein A sepharose resins. Application of OX40L-IgG resulted in healing of leishmania lesions or delaying in development of the lesions in leishmania-infected mice.
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31

Dodd, Will. "Pediatric Rheumatology, Heme-Onc, and Immunology". Digital Commons @ East Tennessee State University, 2020. https://dc.etsu.edu/etsu-works/8912.

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32

Hill, Bruce Derick. "The pathobiology and immunology of cryptosporidiosis". Thesis, University of Edinburgh, 1989. http://hdl.handle.net/1842/30269.

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33

Leber, Andrew James. "Systems Immunology Approaches for Precision Medicine". Diss., Virginia Tech, 2017. http://hdl.handle.net/10919/78233.

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The mucosal immune system encompasses a wide array of interactions that work in concert to protect an individual from harmful agents while retaining tolerance to molecules, microbes, and self-antigens that present no danger. The upheaval in the regulation-response balance is a critical aspect in both infectious and immune-mediated disease. To understand this balance and methods of its restoration, iterative and integrative modeling cycles on the pathogenesis of disease are necessary. In this thesis, I present three studies highlighting phases of a systems immunology cycle. Firstly, the thesis provides a description of the construction of a computational ordinary differential equation based model on the host-pathogen-microbiota interactions during Clostridium difficile infection and the use of this model for the development of the hypothesis that host-antimicrobial peptide production may correlate with increased disease severity and promote increased recurrence. Secondly, it provides insight into the necessity of trans-disciplinary analysis for the understanding of novel molecular targets in disease through the immunometabolic regulation of CD4+ T cell by NLRX1 in inflammatory bowel disease. Third, it provides the assessment of novel therapeutics in disease through the evaluation of LANCL2 activation in influenza virus infection. In total, the computational and experimental strategies used in this dissertation are critical foundational pieces in the framework of precision medicine initiatives that can assist in the diagnosis, understanding, and treatment of disease.
Ph. D.
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34

Doyle, Chloe. "Investigating The Immunology Of Crohn’s Disease". Thesis, The University of Sydney, 2022. https://hdl.handle.net/2123/29965.

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Crohn’s disease is a chronic autoimmune disease characterised by chronic inflammation in the gastrointestinal tract caused by an uncontrolled immune reaction to commensal bacteria. It is steadily increasing in incidence across the globe, especially in young adults. Current treatments act to reduce inflammation but there is no cure. This is because this disease is still poorly understood especially regarding the specific immune cells involved. Defining these cells and their functions could provide critical insights into the causes and progression of this disease and pave the way for therapeutic interventions. Our group has privileged access to large human intestinal explants from patients undergoing surgery to remove Crohn’s affected tissue. We are also experts in the biology of mononuclear phagocytes, which are key cells in mediating immune tolerance and inflammation and represent an obvious class of cells that may play a role in Crohn’s disease. Here we have firstly optimised intestinal tissue digestion protocols to extract mononuclear phagocytes (and other immune cells) from fresh human intestinal tissue in a viable and functional state. We then designed and optimised high-parameter flow cytometry panels to comprehensively identify and characterise all known subsets of mononuclear phagocytes as well as innate lymphoid cells, mucosal-associated invariant T cells, natural killer cells and  T cells. We then accurately defined the mononuclear phagocyte subsets present in tissue affected by Crohn’s Disease compared to uninflamed tissue and inflamed non-Crohn’s tissue. We revealed that langerin+ type-2-conventional dendritic cells (cDC2) were significantly reduced in Crohn’s affected ileum. We went on to show that in healthy tissues these cells drove the induction of CD4+ T helper 2 and T helper 17 cells that highly expressed GATA3, RORt and AHR. Restoration of langerin+ cDC2 in Crohn’s Disease patients may therefore provide a therapeutic avenue to treat this illness.
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35

Ngo, Chinh Chung. "Microbiology and Immunology of Otitis Media". Thesis, Griffith University, 2016. http://hdl.handle.net/10072/365263.

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Background Over 80% of children experience acute otitis media (AOM) at least once during childhood, with 10-30% of children experiencing recurrent episodes of AOM (RAOM) or persistence of fluid in the middle ear (ME) lasting greater than 3 months which is defined as chronic otitis media with effusion (COME). Microbial infection remains the main cause of AOM, however the causes of RAOM and COME are not fully understood. Heavy loads of microbial colonisation and bacterial/viral interaction in the upper respiratory tract (URT) contribute to OM pathogenesis. It is currently unclear whether compromised host immune system responses have a significant role in RAOM/COME. Bacterial biofilms within the ME may contribute to otopathogen persistence and recurrent infection and/or inflammation in these children. Aims This study identified the predominant bacterial and viral otopathogens within the URT and ME, of children undergoing ventilation tube insertion (VTI) for RAOM/COME. Bacterial persistence within the ME, in the form of biofilms was also examined. Bacteria and viruses which were identified within the URT of children with RAOM/COME were compared to a control group of children who were undergoing adenoidectomy for treatment of adenoidal hypertrophy (AH) and/or obstructive sleep apnoea (OSA). Local (saliva, middle ear effusion (MEE)) and systemic (serum) innate and adaptive immune responses were examined in children with and without RAOM/COME. Specific antibody levels to bacterial proteins as well as cytokine levels were determined. Systemic immuno-gene expression was compared between children with RAOM/COME and AH/OSA.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
Griffith Health
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36

Tjärnlund, Anna. "Does IgA play a role in protection against pulmonary tuberculosis?" Licentiate thesis, Stockholm University, Wenner-Gren Institute for Experimental Biology, 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-552.

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More than a century after the identification of the tubercle bacillus and the first attempts at vaccination, tuberculosis (TB) still remains one of the world’s most serious infectious diseases. TB is typically a disease of the lung, which serves both as port of entry and as the major site of disease manifestation. The currently used vaccine, Mycobacterium bovis bacillus Calmette-Guérin (BCG), is administered parentally and induces a systemic immune response. However, it fails to protect against pulmonary TB, thereby raising the question whether vaccination targeting the mucosal immunity in the lungs could be favourable.

The respiratory mucosal surfaces represent the first line of defence against a multitude of pathogens. Secretory IgA (sIgA) in mucosal secretions has an important function by blocking entrance of pathogenic organisms and preventing infections. Yet, another role for IgA in protection against intracellular pathogens has lately been appreciated, when sIgA was demonstrated to neutralize viruses intracellulary. We aimed to investigate the relevance of sIgA in protection against mycobacterial infections using mice deficient for IgA and the polymeric Ig receptor. Mice were immunized intranasally with a mycobacterial antigen which elicited, in wild-type mice, a strong IgA response in mucosal secretions in the respiratory tract. Gene-targeted mice failed to induce the same response and more importantly, were more susceptible to mycobacterial infections in the respiratory tract, as demonstrated by higher bacterial loads in the lungs than wild-type mice. Analysis of immune responses after infection revealed reduced production of proinflammatory, and protective, factors such as IFN-γ and TNF-α in the lungs of deficient mice, which was in concordance with the higher bacterial burden seen in the lungs of these mice. The mechanisms explaining the defective proinflammatory responses in the lungs of deficient mice are not clear but might involve impaired signalling through Fcα receptors, or homologous receptors, which could lead to inadequate activation of pulmonary macrophages. This could subsequently result in suboptimal induction and production of cytokines and chemokines important for attraction and migration of cells to sites of infection in the lungs.

Our results demonstrate a role for IgA in protection against mycobacterial infection in the respiratory tract by blocking the entrance of the mycobacterium into the lungs, and/or by modulating the locally induced proinflammatory immune responses.

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Arko-Mensah, John. "Immune evasion and identification of biomarkers associated with mycobacterial infection". Licentiate thesis, Stockholm University, Wenner-Gren Institute for Experimental Biology, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-7253.

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38

Johansson, Alina. "Molecular mechanisms behind TRIM28expression". Thesis, Uppsala universitet, Institutionen för biologisk grundutbildning, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-252834.

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39

Andersson, Jonas. "Complement Activation Triggered by Biomaterial Surfaces : Mechanisms and Regulation". Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis Univ.-bibl. [distributör], 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3410.

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Mouchtaridi, Elli. "The role of exosomes in sarcoidosis". Thesis, Uppsala universitet, Institutionen för biologisk grundutbildning, 2021. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-446010.

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Sarcoidosis is a systemic inflammatory disease mostly affecting the lungs, marked by the presence of granulomas and the accumulation of interferon gamma (IFNγ)-producing T cells in the affected organs. Extracellular vesicles (EVs) are membranous vesicles with a size range of 50 nm to 5000 nm, with exosomes ranging from 50 to 150 nm. They are major players in intercellular communication and have been found in all body fluids including plasma. In this study, we wanted to characterize the exosomes from sarcoidosis patients’ plasma and try to detect differences in their surface marker expression. Additionally, we aimed to investigate the cellular origin of these exosomes in the blood circulation of mice. We used a combination of Nanoparticle Tracking Analysis (NTA), Transmission Electron Microscopy (TEM), Western Blot and Flow cytometry as characterization methods. Moreover, we took advantage of immune cell-specific knock-out mice (Rag KO, Ly6G-Mcl-1 KO) and examined the effect on the number of vesicles and on the marker expression levels on the vesicle surface. We showed that in Rag KO mice, that lack mature B cells and T cells, the levels of T cell markers CD4 and CD8 were decreased. No difference was detected between wild type and neutrophil KO mice on neither of the neutrophil-specific markers Ly6G and CD11b. Sarcoidosis patient plasma EVs showed lower levels of CD9 expression compared to healthy subjects. Differences were observed in a subgroup of patients, namely Löfgren syndrome patients that exhibited higher CD31 expression than the non-Löfgren patients. Overall, our data indicate a possible contribution of the immune cell-derived exosomes in the blood. Furthermore, differences detected in the sarcoidosis plasma EVs could give a better insight on the role of those exosomes during lung inflammation and provide grounds for their use as liquid tissue biomarkers.
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Mullazehi, Mohammed. "Anti-Collagen Type II Autoantibodies in an Acute Phenotype of Early Rheumatoid Arthritis". Doctoral thesis, Uppsala universitet, Institutionen för onkologi, radiologi och klinisk immunologi, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-100483.

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Rheumatoid arthritis (RA) is an autoimmune disease with systemic inflammatory features that primarily affects small peripheral joints. Type II collagen (CII), is the most abundant collagen type in joint cartilage. Antibodies against CII (anti-CII) are found in a subpopulation of RA patients. Anti-CII can form surface-bound immune complexes (IC) in inflamed joints, which might intensify joint inflammation and destruction. In this thesis I have studied the functional effects of surface-bound anti-CII–containing IC in vitro and correlated the results to clinical parameters. Anti-CII IC induced TNF-α, IL-1β and IL-8 production from monocytes via FcγRIIa. Anti-CII levels were dichotomously distributed in RA patients where a small outlier group (3.3%) with very high anti-CII levels showed in vitro induction of pro-inflammatory cytokines by anti-CII-containing IC. These patients also had a distinct phenotype with elevated laboratory signs of inflammation and increased radiological erosions at the time of diagnosis. In another in vitro model, co-cultured macrophages and RA synovial fibroblasts stimulated with anti-CII IC induced the production of matrix metalloproteinases (MMP)-1 and MMP-8, enzymes responsible for the initial cleavage of CII during cartilage degradation. This was mediated via production of TNF-α and IL-1β, and especially anti-CII IC-induced IL-1β sup-ported the production of MMP-1. The presence of anti-CII antibodies in patients with early synovitis was not predictive for future RA development. In summary, I have shown how anti-CII-containing IC may explain part of the early pathogenesis and can define a distinct clinical phenotype in RA patients with high levels of anti-CII.
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Åhlin, Erik. "Functional Role of Immune Complexes in Rheumatic and Parasitic Diseases". Doctoral thesis, Uppsala universitet, Klinisk immunologi, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-139529.

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Immune complexes (IC) have key pathological roles in both autoimmune and infectious diseases. In this thesis functional mechanisms behind IC-driven inflammation in rheumatic diseases and tropical infections have been studied, with special focus on the contribution of autoantibodies and cytokine-inducing properties of IC. In the autoimmune disease SLE, increased levels of IC-induced cytokines were associated with both increased classical complement activation and the occurrence of the autoantibodies anti-SSA and anti-SSB, both directed against RNA-associated antigens. In addition, complement activation and anti-SSA synergistically predisposed to higher levels of IC in sera. In the following study it was demonstrated that also other autoantibodies against RNA-associated autoantigens were more enriched than anti-dsDNA in SLE IC. Sudanese Visceral Leishmaniasis (VL) patients had elevated IC levels, and precipitated IC induced higher levels of GM-CSF, IL10, IL6 and IL1RA than control IC. Levels of IC were especially prominent in severely ill patients receiving antimony treatment, and a parallel association with IC induction of GM-CSF was demonstrated. Leishmania-infected patients were often rheumatoid factor (RF) positive and a substantial number displayed reactivity towards cyclic citrullinated peptide (CCP) antigens. Contrary to what was seen in Sudanese RA sera, the CCP reactivity was not restricted to citrulline but reacted equally well with arginine-containing control peptides. Levels of anti-CCP among VL patients were not due to cross-reactions with, or CCP-reactivity bound to IC. I have demonstrated that IC are associated with the presence of autoantibodies in both SLE and in Leishmania infection. In SLE, autoantibodies against RNA-associated antigens were more prone to form circulating IC than anti-dsDNA. In Leishmania infection false reactivity against the CCP-autoantigen correlated to IC levels although the IC themselves did not contain such reactivity. In both diseases higher IC levels were associated with a more active disease, and purified IC induced key cytokines in disease pathogeneses.
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Andersson, Josefin. "Utvärdering av Malaria Antigen ELISA kit för diagnostik av malaria vid Christian Medical College and Hospital i Vellore, Indien. : en jämförande studie mellan Quantitative buffy coat och enzyme-linked immunosorbent assays (ELISA) metodik". Thesis, Örebro universitet, Institutionen för hälsovetenskap och medicin, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-4889.

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Malaria är ett globalt hälsoproblem som orsakar många dödsfall runt om i världen varje år och nästan hälften av jordens befolkning ligger i riskzonen att drabbas av sjukdomen. I Indien drabbas mellan 2-3 miljoner människor varje år och det inträffar omkring 900 dödsfall. Malaria orsakas av Plasmodium sp. som är en protozoe, och det finns fyra olika arter som är patogena för människor, P. vivax, P. ovale, P. falciparium samt P. malariae. Vanliga metoder för att diagnostisera malaria är genom tunna och tjocka blodutstryk som färgas till exempel med Giemsa, Fields eller Leishmans färgningsteknik och studeras mikroskopiskt, Quantitative Buffy Coat (QBC), PCR tester, acridinorange färgning samt olika immunologiska tester för detektion av antikroppar eller antigen som till exempel enzyme-linked immunosorbent assays (ELISA) test och dipstick test. Syftet med denna studie är att utvärdera om en användning av SD Bio Line Malaria Antigen ELISA kit ger en mer känslig, tillförlitlig, praktisk samt mindre kostsam diagnostikmetod för malaria hos patienter med misstänkt malariainfektion än den nuvarande guldstandardmetoden, QBC tillsammans med blodutstryk, vid Christian Medical College and Hospital i Vellore. Patientproverna har i både ELISA testet samt QBC testet tillsammans med utstryk erhållit samma resultat vilket tyder på att SD Bio Line Malaria Antigen ELISA kitet skulle kunna vara en lika bra diagnostikmetod som QBC testet för diagnos av malaria. ELISA kitet har dock fler nackdelar, i jämförelse med QBC testet, så därför är slutsatsen att SD Bio Line Malaria Antigen ELISA kitet inte är en mer lämplig diagnostisk metod för malaria än den som används vid CMCH. Men då ELISA testet ändå ger en säker diagnos, enligt resultatet i studien, kan den vara ett lämpligt test inom något annat användningsområde.
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44

Martin, Melina Toni Marie. "The effects of probiotic and dietary fiber administration on intestinal physiological markers in pigs". Thesis, Uppsala universitet, Institutionen för biologisk grundutbildning, 2020. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-416249.

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45

Lindroth, Karin. "Maturation of humoral immune responses : Studies on the effects of antigen type, apoptosis and age". Doctoral thesis, Stockholm : Wenner-Grens institut, Univ, 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-85.

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46

Douguet, Laetitia. "Conséquences de l’expression de la synthétase de l’oxyde nitrique de type 2 (NOS2) sur les fonctions des lymphocytes T γδ au cours du développement du mélanome". Thesis, Sorbonne Paris Cité, 2015. http://www.theses.fr/2015USPCB106/document.

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Au cours du développement d’un cancer, la tumeur se forme dans un environnement adapté à sa croissance appelé microenvironnement tumoral. Celui-ci est constitué d’un réseau complexe qui orchestre la progression tumorale et dans lequel sont présents différents types cellulaires, des facteurs solubles ainsi que des composants de la matrice extracellulaire. Parmi les cellules du microenvironnement tumoral, on trouve les cellules du système immunitaire. Certaines ont la capacité de reconnaître et d’éliminer directement les cellules cancéreuses, tandis que d’autres promeuvent la croissance tumorale et la dissémination métastatique. Les lymphocytes T γδ ont longtemps été considérés uniquement comme des acteurs anti-tumoraux, agissant grâce à leur fonction cytotoxique et à leur sécrétion précoce d’interféron (IFN)-γ. Dans de plus en plus de travaux récents, l’idée que les lymphocytes T γδ soient, également, des acteurs pro-tumoraux est mise en évidence. Leurs fonctions pro-tumorales sont principalement attribuées à leur production d’interleukine (IL)-17, favorisant l’angiogenèse et le recrutement de cellules myéloïdes suppressives (MDSCs). Le mécanisme induisant la polarisation des T γδ vers la production d’IL-17 plutôt que d’IFN-γ restait à préciser. Nous avons identifié la synthétase de l’oxyde nitrique de type 2 (NOS2) comme candidat potentiel étant donné son action exercée sur la production d’IL-17 par les lymphocytes T αβ CD4+ (Th17). Nous montrons que les cellules T γδ expriment NOS2 dans les tumeurs primaires de mélanome chez les patients et également chez la souris, dans un modèle de développement spontané de mélanome. Nous avons identifié que l’expression de NOS2 endogène était un inducteur clé de la sécrétion d’IL-17 par les T γδ dans le mélanome, ce qui a pour conséquence de recruter les MDSCs dans la tumeur primaire et d’induire la dissémination métastatique. En parallèle, les T γδ exprimant NOS2 produisent moins d’IFN-γ et présentent, in vitro, des capacités de lyse des cellules tumorales réduites en comparaison avec les T γδ déficients pour NOS2. Nous émettons l’hypothèse que le microenvironnement tumoral puisse fournir les facteurs nécessaires à l’activation des T γδ (comme l’IL-1β, l’IL-6 et ou la reconnaissance d’un antigène par le TCR) pour permettre l’expression endogène de NOS2 par les cellules T γδ. En plus de favoriser la polarisation des T γδ en effecteurs pro-tumoraux, nous montrons que NOS2 favorise leur expansion par un mécanisme dépendant de l’IL-2. En effet, les T γδ déficients pour NOS2 montrent des capacités de prolifération et un métabolisme glycolytique réduits qui sont restaurés par l’ajout d’IL-2 exogène
Consequences of the expression of nitric oxide synthetase type 2 (NOS2) on the functions of γδ T lymphocytes during the development of melanoma
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47

Wirth, Monika. "Immunology of the genital tract - a review". Diss., lmu, 2007. http://nbn-resolving.de/urn:nbn:de:bvb:19-68316.

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48

Cozzi, E. "The immunology of pig-to-primate xenotransplantation". Thesis, University of Cambridge, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.598114.

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This thesis describes the analysis of transgenic pigs expressing the human regulatory protein decay-accelerating factor (HDAF). The first part of this research was aimed at proving the success of the genetic manipulation undertaken, by demonstrating the existence of HDAF in these transgenic pigs. These studies, conducted on PBMC from founder animals, provided evidence that both lymphocytes and monocytes from most transgenic pigs analysed express the HDAF protein. As altered expression and function of human proteins in transgenic pigs had previously been reported, the HDAF was further characterised by immunoprecipitation and epitope mapping. Together these experiments demonstrated the integrity of HDAF expressed by these transgenic pigs. To test the efficacy of the transgene, HDAF transgenic pig hearts were heterotopically transplanted into cynomolgus monkeys. None of these organs underwent HAR demonstrating the capacity of HDAF to protect the xenograft from complement mediated damage. HDAF transgenic pig kidneys were also transplanted into immunosuppressed and splenectomised cynomolgus monkeys. This led to a prolongation in the survival time of primates receiving a life-supporting porcine renal xenograft. The final part of this thesis provides insight into the xenogeneic antibody repertoire believed to be responsible for the vascular rejection of these transgenic organs. In conclusion, the detailed characterisation of the recently developed HDAF transgenic pig lines has led to the identification of pigs whose organs are not hyperacutely rejected when transplanted into primates. Together with growing insight into the humoral mechanisms responsible for the onset of delayed graft rejection, these studies have led to the longest survival reported to date for recipients of life-supporting pig-to-primate renal transplants.
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49

Yang, Demao. "Immunology of membrane proteins of Leishmania major". Thesis, Open University, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.304854.

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50

Mair, T. S. "Respiratory immunology and hypersensitivity in the horse". Thesis, University of Bristol, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.370896.

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