Dissertationen: „CD antigens“

1

Osorio, Fernández Lyda María. „Regulation of T-cell proliferation and B-CLL apoptosis by CD6 and FAS/FASL /“. Stockholm, 1998. http://diss.kib.ki.se/search/diss.se.cfm?19980605osor.

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2

Fernvik, Eva C. „Cell biological mechanisms and activity markers of eosinophils in relation to allergic inflammation /“. Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3399-5/.

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3

Varelias, Antiopi. „Studies of CD44 variant isoform expression and function on activated human peripheral blood mononuclear cells and in renal transplantation“. Title page, summary and contents only, 2001. http://web4.library.adelaide.edu.au/theses/09PH/09phv293.pdf.

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4

Walter, Roland Bruno. „Mechanism of endocytosis of CD33/Siglec-3 : role of ITIMs, tyrosine phosphorylation, and monoubiquitylation /“. Thesis, Connect to this title online; UW restricted, 2006. http://hdl.handle.net/1773/6325.

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5

Otipoby, Kevin L. „CD22 regulates B cell fate via two signaling domains within its cytoplasmic tail /“. Thesis, Connect to this title online; UW restricted, 2000. http://hdl.handle.net/1773/8335.

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6

Misztela, Dominika. „The differential effects of CD80 and CD86 in helper T lymphocyte activation“. Thesis, University of Oxford, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.670088.

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7

Cheung, Chi-ho, und 張志豪. „Identification of CD47 as a novel therapeutic target for hepatocellular carcinoma“. Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B46945374.

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8

Dai, Tong. „Differential role of CEACAM1 and CEACAM2 in insulin metabolism“. Connect to full-text via OhioLINK ETD Center, 2004. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=mco1139336269.

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Thesis (Ph.D.)--Medical University of Ohio, 2004.
"In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Medical Sciences." Major advisor: Sonia M. Najjar. Includes abstract. Document formatted into pages: v, 217 p. Title from title page of PDF document. Bibliography: pages 158-216.

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9

Haas, Karen M. „Induction and regulation of bovine B lymphocyte responses“. free to MU campus, to others for purchase, 2000. http://wwwlib.umi.com/cr/mo/fullcit?p9999290.

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10

Daoud, Roni N. „A study of MRP1-drug interactions : identification of the drug binding site(s)“. Thesis, McGill University, 2000. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=36801.

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Over-expression of either P-gp1 and/or MRP1 in tumor cell lines confers resistance to structurally diverse anti-cancer drugs. Although the role of these two proteins in clinical drug resistance remains to be confirmed, the use of Pgp1-specific inhibitors in combination with standard anti-cancer drugs have demonstrated significant improvement in clinical response. However, evidence exists that reversal of P-gp1 alone is not sufficient. Therefore, while no drugs are currently available that can efficiently reverse MRP1 drug efflux in tumor cells, there is an urgent need to develop MRP1-specific blockers. In an effort to gain a better understanding of MRP1-drug interactions and to identify sequences within MRP1 that interact directly with drugs, we developed two structurally diverse photosensitive drug analogues, a quinoline-based compound (IACI) and a xanthone-derivative (IAARh123). Both compounds photolabeled MRP1 and showed a direct and specific interaction with the protein at physiologically relevant sites. Initial mapping of photolabeled sequences in MRP1 (Chapters 2 and 3), identified multiple IACI- or IAARh123-photolabeled peptides (∼4--7 kDa) derived from both the N-terminal (MSD0+MSD1+NBD 1) and C-terminal (MSD2+NBD2) domains of MRP1. A subsequent study (Chapter 4), using MRP1 variants with hemagglutinin (HA) epitopes inserted at eight different locations, led to a higher resolution mapping of the previously identified IACI- or IAARh123-labeled peptides. Specifically, two photolabeled peptides (∼6--7 kDa), derived from variants with insertions at positions 574 and 1222, were immunoprecipitated with anti-HA monoclonal antibody. Based on the location of the HA epitopes in the latter variants together with molecular masses of the two peptides, the photolabeled amino acid residues were localized to MRP1 sequences encoding transmembranes 10 and 11 of MSD1 and transmembranes 16 and 17 of MSD 2. Interestingly, the same sequences were photolabeled with both

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11

Peterson, Karin E. „The role of secondary signaling in experimental autoimmune thyroiditis“. free to MU campus, to others for purchase, 1998. http://wwwlib.umi.com/cr/mo/fullcit?p9904865.

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12

Ong, Yen May. „The role of [Beta]1-integrins in centrosomal stability /“. Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111566.

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Centrosomes are major microtubule organizing centres that set up an internal microtubule (MT) network contributing to cell shape and to the formation of the mitotic spindle during cell division. Rearrangement of this MT array can be dictated by the centrosome and occurs during cell adhesion, polarization and migration. However, little is known about what regulates centrosome assembly and maintenance. beta1-integrins are common cell surface receptors and we show that beta1-integrin signalling is necessary for modulation of centrosome dynamics. In an attempt to identify the downstream components of beta1-integrin signalling involved, we also discovered that the activation of focal adhesion kinase or integrin linked kinase are not required in maintaining centrosome integrity. This would indicate that a non-canonical signalling beta1-integrin pathway might be involved in controlling centrosomal dynamics. This gives us greater insight into the mechanisms that control centrosomal stability and may lead to the better understanding of diseases like cancer and diseases, i.e. lissencephaly, which involve defects in cell polarization and asymmetric cell division, where the centrosome seems to have an important role.

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13

Yang, Yan. „CEACAM1 : a molecular link between fat metabolism and insulin clearance“. Connect to full-text via OhioLINK ETD Center, 2004. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=mco1115060085.

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Thesis (Ph.D.)--Medical College of Ohio, 2004.
In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Medical Sciences. Major advisor: Sonia Najjar. Includes abstract. Document formatted into pages: v, 167 p. Bibliography: pages 117-165.

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14

Chan, Ping-lung, und 陳秉隆. „Roles of TLR5 and ICOS on the human allogenic CD40-activated B cell-induced CD4hiCD25+ regulatory T cells“. Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B47149735.

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15

Orubu, Toritse. „Generation of multivalent recombinant MVA vaccines for malaria“. Thesis, University of Oxford, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.589603.

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Modified vaccinia virus Ankara (MVA) has been used extensively as a recombinant vector for delivery of antigens from diverse pathogens. Its ability to generate strong antigen specific CD8+ T cell responses in humans has been shown in clinical trials of novel vaccines against malaria, tuberculosis, HIV I AIDS, influenza and cancer. The work in this thesis describes the use of BAC recombineering technology to harness the endogenous regulatory signal (promoter) that drives the expression of non-essential open reading frames (ORFs) in MVA for immunogenic expression of a recombinant antigen. Replacement of the ORFs of four non-essential genes in MVA; C11R, F11l, A44L and B8R with an epitope tagged luciferase positioned to use the same endogenous promoter showed early transgene expression equal to or slightly higher than traditional p7.5 and short synthetic promoter (SSP) constructs. The frequency of antigen-specific CD8+ T cell induced in mice by single dose MVA or adenovirus-prime, rMVA-boost vaccination showed equivalent or slightly higher responses by the endogenous promoters compared to the traditional p7.5 and SSP constructs. Assessment of the growth rate of these viruses showed they were unimpaired and the insertions were genetically stable. Furthermore, the endogenous promoter driven insertion loci of B8R and C11R were used for the construction of a bivalent MVA expressing an epitope tagged luciferase (rLucPb9) and a Photinus pyralis (pLuc) luciferase. The frequency of antigen-specific CD8+ T cells induced in mice by bivalent MV A was equivalent to single-pLuc and single-Pb9 recombinants co-administered as a mixture, at separate sites or administered alone following single dose MV A vaccination but slightly lower for Pb9-specific CD8+ T cell following adenovirus-prime, rMVA-boost.

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16

Sundberg, Ulla. „Differential expression pattern of CEACAM1 isoforms in polarized epithelial cells, its regulation and some functional consequences /“. Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-774-6/.

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17

Lee, Jai-Wei 1970. „Application of soluble CD14 and a trivalent vaccine to prevent mastitis caused by Escherichia coli and Staphylococcus aureus“. Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=84455.

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Escherichia coli (E. coli) and Staphylococcus aureus (S. aureus) are the most prevalent pathogens to induce mastitis. The pathogenesis of infections induced by E. coli is sophisticatedly modulated by lipopolysaccharide (LPS), LPS binding protein, membrane CD14 (mCD14), and soluble CD14 (sCD14). In the first study, administration of recombinant bovine sCD14 (rbosCDl4) significantly reduced the fatality of LPS challenged mice and the severity of mouse mastitis in terms of clinical signs, bacterial load, and TNF-alpha production. Before investigating the potential of this strategy in dairy cows, endogenous sCD14 in milk was characterized. Based on the data of 396 quarters, the milk concentration of sCD14 was 6.67 +/- 0.44 mug/ml. The stages of lactation affected the concentration of sCD14 in milk, which was higher in transitional milk (0--4 days postpartum). Milk sCD14 also increased during an intramammary LPS challenge, which paralleled with SCC increase. The protective effect of sCD14 on bovine E. coli mastitis was then investigated. It was shown that rbosCDl4 sensitized the mammary gland to recruit leukocytes in response to LPS. To prove that the early recruitment of leukocytes plays a role in preventing intramammary E. coli infections, E. coli mastitis was induced in 9 dairy cows with or without 100 mug rbosCD14. Quarters challenged with E. coli plus rbosCD14 had a more rapid recruitment of neutrophils, a faster clearance of bacteria, reduced concentrations of TNF-alpha and IL-8 in milk, and reduced clinical symptoms than quarters injected with saline.
For S. aureus mastitis, a newly designed trivalent whole-cell vaccine being composed of the most dominant serotypes (T5, T8, and T336) was evaluated. The vaccine was immunized with or without either one of the two adjuvants, aluminum hydroxide (ALUM) and Freund's incomplete adjuvant (FICA). The vaccine, with or without the presence of adjuvants, increased antigen-specific IgG1, IgG2, but not IgM, in serum. However, all formulations only had limited effects on lymphocyte subsets, interferon (IFN)-gamma mRNA expression, and neutrophil phagocytosis in comparison with the control.
Taken together, the results indicated that increasing the concentration of sCD14 in milk might be a potential strategy to prevent or reduce severity of E. coli mastitis. On the other hand, both ALUM and FICA did not augment the immune responses when formulated with trivalent vaccine. A more immunostimulatory adjuvant will be required to improve the efficacy of the novel trivalent vaccine against S. aureus mastitis.

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18

Lundmark, Frida. „Genetic analysis of IL7R and other immune-regulatory genes in multiple sclerosis /“. Stockholm : Karolinska institutet, 2007. http://diss.kib.ki.se/2007/978-91-7357-278-1/.

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19

Leicester, Katherine L. „Characterization of the role of CD14 in human and animal liver diseases /“. Connect to this title, 2004. http://theses.library.uwa.edu.au/adt-WU2005.0109.

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20

Lee, Ping-yin, und 李炳賢. „Expression and mutations of fas gene in oesophageal cancer“. Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B31971155.

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21

Quan, Jun-Min. „Theoretical studies of biomacromolecules : collagen, collagen-like peptides & HIV-1 envelope glycoprotein GP120 /“. View abstract or full-text, 2004. http://library.ust.hk/cgi/db/thesis.pl?CHEM%202004%20QUAN.

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22

Rahmatpanah, Farahnaz B. Caldwell Charles W. „Large scale CpG island methylation profiling of small B cell lymphoma“. Diss., Columbia, Mo. : University of Missouri-Columbia, 2008. http://hdl.handle.net/10355/6863.

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

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23

Heinrich, Garrett. „A role for CEACAM proteins in energy balance and peripheral insulin action“. Toledo, Ohio : University of Toledo, 2010. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=mco1272976279.

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Dissertation (Ph.D.)--University of Toledo, 2010.
"Submitted to the Graduate Faculty as partial fulfillment of the requirements for the Doctor of Philosophy Degree in Biomedical Sciences." Title from title page of PDF document. "A Dissertation entitled"--at head of file. Bibliography: p. 37-41, 77-82, 102-107, 124-125, 153-160, 195-199, 221-254.

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24

Bernatchez, Emilie. „CD103-mediated regulation of airway hypersensitivity responses to bioaerosol-associated antigens“. Doctoral thesis, Université Laval, 2018. http://hdl.handle.net/20.500.11794/30253.

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Les mécanismes immunitaires impliqués dans le maintien de l’homéostasie pulmonaire sont finement régulés étant donné l’exposition constante des voies aériennes aux bioaérosols. Plusieurs cellules participent au maintien de l’homéostasie pulmonaire, telles les cellules dendritiques. Un sous-type de cellules dendritiques pulmonaires attire particulièrement l’attention dans l’homéostasie pulmonaire, les cellules dendritiques CD103+, étant donné qu’il a été démontré qu’elles participent dans la tolérance immune. Toutefois, ce rôle reste controversé, car des études démontrent qu’elles participent plutôt au développement de réponses inflammatoires pulmonaires. De plus, le CD103 (une intégrine exprimée par des sous-types de cellules dendritiques et de lymphocytes T), est surtout utilisé comme marqueur cellulaire et le rôle spécifique joué par l’expression du CD103 sur ces cellules reste inconnu. L’homéostasie pulmonaire n’est pas toujours maintenue. Chez des individus susceptibles, l’exposition aux bioaérosols peut mener au développement de réponses inflammatoires. C’est le cas pour l’asthme et l’alvéolite allergique extrinsèque, deux réponses d’hypersensibilités pulmonaires, de type I et de type mixte III/IV respectivement. Récemment, des espèces d’archées, Methanosphaera stadtmanae (MSS) et Methanobrevibacter smithii (MBS), ont été retrouvées en grande concentration dans les bioaérosols d’environnements agricoles et il a été démontré que l’exposition pulmonaire à leur extrait mène au développement d’une réponse immune chez la souris. Toutefois, le type de réponse d’hypersensibilité pulmonaire qu’elles induisent reste méconnu, une information cruciale qui permettra la poursuite de la recherche sur leur potentiel d’induire une réponse pulmonaire chez l’humain. De plus, même si plusieurs thérapies contre les maladies d’hypersensibilité pulmonaires existent, ce ne sont pas tous les sous-groupes de patients qui répondent à la médication, menant à des conséquences socio-économiques importantes pour le système de santé et pour les patients. Ainsi, il demeure important de poursuivre la recherche sur de potentielles cibles thérapeutiques, telles les cellules impliquées dans le maintien de l’homéostasie pulmonaire. Cette thèse vise donc à évaluer le rôle de l’expression du CD103 dans le maintien de l’homéostasie pulmonaire dans le contexte de maladies d’hypersensibilité pulmonaires induites par des antigènes retrouvés dans les bioaérosols. Le rôle de l’expression du CD103 dans l’hypersensibilité de type I induite par l’ovalbumine ou l’extrait d’acariens (modèles d’asthme) a d’abord été a évalué via l’utilisation de souris Cd103-/-. Nous démontrons que l’expression du CD103 est cruciale pour le contrôle de la sévérité de l’inflammation pulmonaire et qu’elle pourrait être impliquée dans l’initiation de la phase de résolution de la réponse inflammatoire. De plus, l’expression du CD103 sur les cellules dendritiques joue un rôle dans leur migration aux ganglions lymphatiques. Ensuite, nous avons évalué le rôle de l’expression du CD103 dans la réponse d’hypersensibilité de type mixte III/IV en réponse à Saccharopolyspora rectivirgula (SR; modèle d’alvéolite allergique extrinsèque) en utilisant des souris Cd103-/-. De plus, en utilisant des modèles de transfert de cellules, nous avons évalué le rôle de l’expression du CD103 dans la réponse au SR lorsque seulement exprimé par les cellules dendritiques ou seulement par les lymphocytes T CD4. Nous démontrons que c’est l’expression du CD103 sur les cellules dendritiques spécifiquement qui est impliquée dans la régulation de l’initiation de la réponse inflammatoire. Après avoir déterminé le type de réponse d’hypersensibilité induite par l’extrait de MSS ou MBS, nous avons étudié le rôle de l’expression du CD103 en réponse à ces archées. Nous démontrons que l’exposition à MSS induit une réponse immune typique d’une hypersensibilité pulmonaire de type IV. Les résultats obtenus après l’exposition à MBS indiquent aussi que la réponse développée est une hypersensibilité de type IV, même si cela reste à confirmer. Finalement, étant donné une grande variabilité entre nos expériences chez les souris Cd103-/-, nous n’avons pu obtenir de conclusion sur le rôle de l’expression du CD103 dans les réponses d’hypersensibilités induites par les archées. Ces résultats démontrent que l’expression du CD103 sur les cellules dendritiques joue un rôle dans le contrôle de l’homéostasie pulmonaire en réponse à des bioaérosols spécifiques qui induisent une hypersensibilité pulmonaire. Les mécanismes exacts régulés par le CD103 sur les cellules dendritiques menant au maintien de l’homéostasie pulmonaire restent à être élucidé. De plus, nos résultats confirment que les espèces d’archées MSS et MBS induisent chacune une réponse d’hypersensibilité pulmonaire qui lui est spécifique, des résultats qui contribueront à déterminer si ces microorganismes induisent une pathologie chez l’Homme.
As we breathe, the lungs are constantly exposed to bioaerosols that challenge the maintenance of airway homeostasis. Many cells are involved in the maintenance of lung homeostasis, such as airway dendritic cells (DCs). A subset of airway DCs has gained special interest in the past years for its role in immune tolerance: CD103+ DCs. Yet, this role remains controversial as there are also reports that they induce airway inflammatory responses. Furthermore, CD103 (an integrin expressed by subsets of DCs and T cells) is mostly used as a marker and whether CD103 expression on these cells plays a specific role remains unknown. Airway homeostasis is not always maintained. Exposure to bioaerosols can elicit an immune response in susceptible individuals, such as in asthma and hypersensitivity pneumonitis, two common airway hypersensitivity diseases of type I and mixed type III/IV hypersensitivity, respectively. Recently, archaea species Methanosphaera stadtmanae (MSS) and Methanobrevibacter smithii (MBS) were identified in high concentrations in bioaerosols from agricultural environments and their extracts were shown to induce an immune response in the airways of mice. However, the type of airway hypersensitivity response they induce remains unknown, a key information that is required if research is pursued on whether they elicit an airway hypersensitivity response in humans. Furthermore, although many therapies for airway hypersensitivity diseases exist, not all subsets of patients respond to the current medication, resulting in high social and economic impacts on the health system and patients. Therefore, research on potential therapy targets for airway hypersensitivity diseases, such as those involved in the maintenance of airway homeostasis, remains important. This thesis focuses on the role of CD103 expression in the maintenance of lung homeostasis in the context of airway hypersensitivity responses induced by antigens found in bioaerosols. We first assessed the role of CD103 expression in type I hypersensitivity in response to ovalbumin or house dust mite extract (models of experimental asthma) using Cd103-/- mice. We found that CD103 expression is crucial in controlling the severity of airway inflammation and could be involved in initiating the resolution of the inflammatory response. Furthermore, CD103 expression on DCs regulates DC trafficking to the draining lymph nodes. We then assessed the role for CD103 expression in mixed type III/IV hypersensitivity in response to Saccharopolyspora rectivirgula extract (SR; model of experimental hypersensitivity pneumonitis) using Cd103-/- mice. Furthermore, using models of cell transfers, we evaluated the role for CD103 expression in the response to SR when specifically expressed by dendritic cells or specifically by CD4 T cells. We demonstrate that CD103 expression on DCs specifically is involved in regulating the onset of the inflammatory response. We finally studied the role for CD103 expression in response to the airway exposure of MSS and MBS extracts, after elucidating the type of hypersensitivity response they induce. We demonstrate that exposure to MSS induces a typical type IV hypersensitivity response. The results obtained after exposure to MBS also indicate development of a type IV hypersensitivity response, although it remains to be confirmed. Finally, due to high variability in the results using Cd103-/- mice, we were unable to reach a conclusion on the role for CD103 expression in response to archaea species. These results demonstrate that CD103 expression by DCs is involved in the control of airway homeostasis to specific airway hypersensitivity-inducing bioaerosols. The exact mechanisms regulated by CD103 on DCs leading to the maintenance of airway homeostasis remain to be elucidated. Furthermore, our results confirm that archaea species MSS and MBS induce a specific type of hypersensitivity response, which will contribute to the elucidation of whether they induce an airway pathology in humans.

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25

Hellström, Martin. „Hyaluronan and the receptor CD 44 in the heart and vessels : a study in normal and pathological conditions /“. Umeå : Univ, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1128.

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26

Lee, Ping-yin. „Expression and mutations of fas gene in oesophageal cancer“. Click to view the E-thesis via HKUTO, 2003. http://sunzi.lib.hku.hk/hkuto/record/B31971155.

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27

Jackson, Leila J. „The dynamic regulation of the low affinity IGE receptor by toll like receptor and B cell receptor agonists /“. Connect to full text via ProQuest. Limited to UCD Anschutz Medical Campus, 2008.

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Thesis (Ph.D. in Immunology) -- University of Colorado Denver, 2008.
Typescript. Includes bibliographical references (leaves 122-129). Free to UCD Anschutz Medical Campus. Online version available via ProQuest Digital Dissertations;

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28

Lundin, Jeanette. „Targeted CD52 therapy in lymphoid malignancies : a clinical and immunological study /“. Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-441-0/.

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29

Lo, Jessica, und 盧姵岐. „Functional characterization and therapeutic implication of CD47 in sorafenib resistance in hepatocellular carcinoma“. Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/208547.

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30

Fernandez, Sonia. „CD4⁺ T-cell deficiency and dysfunction in HIV patients receiving combination antiretroviral therapy /“. Connect to this title, 2006. http://theses.library.uwa.edu.au/adt-WU2007.0120.

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31

MacKenzie, Jason Roderick. „The role of eosinophils in the regulation of CD4+ T helper 2 regulated inflammation /“. View thesis entry in Australian Digital Theses Program, 2004. http://thesis.anu.edu.au/public/adt-ANU20051007.121844/index.html.

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32

Abou-Rjaily, George A. „CEACAM1 links metabolism to epidermal growth factor receptor-mediated cell proliferation“. Connect to full-text via OhioLINK ETD Center, 2004. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=mco1107352295.

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Thesis (Ph. D.)--Medical College of Ohio, 2004.
"In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Medical Sciences." Major advisor: Sonia Najjar. Includes abstract. Document formatted into pages: iv, 181 p. Title from title page of PDF document Includes bibliographical references (p. 123-180).

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33

Sigmundsson, Kristmundur. „Characterization and modelling of CEACAM1 interactions in cell signalling /“. Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-838-6/.

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34

Edelmann, Kurt H. „Murine T cell immunity to primary herpes simplex virus infection : roles for costimulation and MHC class I antigen presentation /“. Thesis, Connect to this title online; UW restricted, 2001. http://hdl.handle.net/1773/5037.

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35

Nopp, Anna. „Characterisation of eosinophil activity markers : relation to allergic inflammation and apoptosis /“. Stockholm : Karolinska Univ. Press, 2002. http://diss.kib.ki.se/2002/91-7349-129-2.

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36

Al-Share, Qusai Y. „Reduction of hepatic CEACAM1 levels : an early mechanism of insulin resistance induced by high-fat diet“. Connect to full text in OhioLINK ETD Center, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=mco1201787222.

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Dissertation (Ph.D.)--University of Toledo, 2007.
"In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Biomedical Sciences." Title from title page of PDF document. Bibliography: p. 120-176.

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37

Dugger, Kari J. „Visualizing the function and migration of T cells“. Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2007. https://www.mhsl.uab.edu/dt/2007p/dugger.pdf.

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38

Alvares, Stacy M. „The role of membrane microdomains in the phosphorylation of the epithelial transmembrane protein, GP140/CDCP1 /“. Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/5022.

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39

Zarling, Angela Lee. „Presentation to and priming of human cd8⁺ T lymphocytes“. free to MU campus, to others for purchase, 1999. http://wwwlib.umi.com/cr/mo/fullcit?p9946319.

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Aniansson, Zdolsek Helena. „Maturation of T lymphocytes and monocytes in children in relation to development of atopic disease /“. Linköping : Univ, 2002. http://www.bibl.liu.se/liupubl/disp/disp2002/med752s.pdf.

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41

Lee, Sang Jun. „CEACAM1 : a common regulator of fat metabolism and cell proliferation“. Connect to full text in OhioLINK ETD Center, 2008. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=mco1218146004.

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Dissertation (Ph.D.)--University of Toledo, 2008.
"In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Biomedical Sciences." Title from title page of PDF document. Bibliography: p. 74-82, 116-124, 146-192.

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Leicester, Katherine L. „Characterization of the role of CD14 in human and animal liver diseases“. University of Western Australia. School of Medicine and Pharmacology, 2005. http://theses.library.uwa.edu.au/adt-WU2005.0109.

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[Truncated abstract] Chronic liver injury results from many etiologies ranging from viral infection to inborn errors of metabolism. A common result of liver injury is activation of hepatic stellate cells and portal fibroblasts to myofibroblasts. In chronic injury, production of extracellular matrix by activated myofibroblasts results in liver fibrosis and ultimately cirrhosis. Kupffer cells and monocytes may play an important role in the pathogenesis of certain liver diseases. Endotoxin-responsive macrophages and recruited monocytes (CD14-positive cells) are potential sources of profibrogenic factors but their potential role in the pathogenesis of liver disease has not previously been examined. The first aim of this thesis described in chapter 3 was to evaluate the hypothesis that CD14-positive macrophages/monocytes are present in the livers of patients with hereditary haemochromatosis (HH), primary biliary cirrhosis (PBC), chronic hepatitis C (HCV) and nonalcoholic steatohepatitis (NASH) and contribute to the pathogenesis of fibrosis as evidenced by co-localization of these cells with activated myofibroblasts. Liver specimens from control subjects and those with HH, PBC, HCV and NASH were immunostained for CD14, CD68 and α-smooth muscle actin and the number of cells expressing these antigens was determined. The total number of hepatic CD68-positive cells was similar in diseased and control livers. The number of CD14-positive cells correlated with advanced fibrosis in HH, PBC, HCV but not in NASH. The number of CD14-positive cells was increased with advanced inflammatory activity in HCV. CD14-positive cells were often associated with α-smooth muscle actin-positive myofibroblasts in fibrous septa. In conclusion, many forms of human chronic liver disease demonstrate increased numbers of CD14-positive macrophages/monocytes which are associated with fibrous septa and myofibroblasts. To determine whether CD14-positive cells contribute to fibrogenesis, experimental models of liver injury were used in chapters 5 and 6. The aim of chapter 5 was to determine whether CD14-positive macrophages/monocytes are detected in a bile duct ligation model of liver injury. To accomplish this aim, a novel antibody to rat CD14 was developed as described in chapter 4. A time-course study was undertaken in rats following bile duct ligation for up to 14 days. An increase in the number of hepatic CD14-positive cells was detected early following bile duct ligation, and was associated with increased gene expression of α-smooth muscle actin and procollagen I. Thus, myofibroblastic transformation in this model was associated with increased numbers of CD14-positive cells suggesting a possible relationship between the two phenomena. In order to specifically evaluate the role of CD14 in myofibroblastic transformation, a final study in CD14 knockout (KO) mice was undertaken in chapter 6

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43

Hirano, Ayumi. „T dependent B cell help in cattle : immunoregulatory function of interleukin-4 and CD40-CD40L interactions /“. free to MU campus, to others for purchase, 1997. http://wwwlib.umi.com/cr/mo/fullcit?p9841150.

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Akimana, Christine. „Structural and Functional Analysis of Moraxella catarrhalis Adhesins MCAP and OMPCD“. University of Toledo Health Science Campus / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=mco1180025995.

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DeAngelis, Anthony Michael. „CEACAM1 : a link between insulin and lipid metabolism“. Connect to full text in OhioLINK ETD Center, 2009. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=mco1243943993.

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Dissertation (Ph.D.)--University of Toledo, 2009.
"In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Biomedical Sciences." Title from title page of PDF document. Bibliography: p. 57-61, p. 20-145.

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Wahle, Joseph A. „Signaling in natural killer cells : SHIP, 2B4 and the Kinome“. [Tampa, Fla] : University of South Florida, 2007. http://purl.fcla.edu/usf/dc/et/SFE0002182.

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Sakthivel, Priya. „Co-stimulatory molecules : genes to protein in autoimmune and inflammatory disorders /“. Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-425-9/.

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Woodard-Grice, Alencia V. „Hyposialylation regulates [alpha]4[beta]1 integrin binding to VCAM-1“. Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2008. https://www.mhsl.uab.edu/dt/2009r/woodard.pdf.

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49

Oliveira, Levindo Alves de [UNIFESP]. „Relação da imunoexpressão de CD10 e NM23 com as características anatomopatológicas e prognósticos do carcinoma colorretal“. Universidade Federal de São Paulo (UNIFESP), 2009. http://repositorio.unifesp.br/handle/11600/10024.

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Made available in DSpace on 2015-07-22T20:50:43Z (GMT). No. of bitstreams: 0 Previous issue date: 2009-05-27. Added 1 bitstream(s) on 2015-08-11T03:25:25Z : No. of bitstreams: 1 Publico-00212.pdf: 1245886 bytes, checksum: 4848d0e58992c5a9ff4b387a14c2534a (MD5)
Objetivos: Analisar a expressão das proteínas CD10 e NM23 por estudo imunohistoquímico do tecido do carcinoma colorretal e da mucosa adjacente. Avaliar a relação da expressão dessas proteínas com os aspectos anatomopatológicos da neoplasia, estadiamento clínico, ocorrência de metástases hepáticas e prognóstico dos doentes. Método: Cento e trinta doentes operados por carcinoma colorretal foram analisados. Bloco de tissue microarray foi confeccionado com tecido neoplásico e com a mucosa não neoplásica adjacente. Estudo imuno-histoquímico foi realizado com anticorpos monoclonais NM23 e CD10 no tecido neoplásico e no tecido não neoplásico da mucosa adjacente. A leitura foi realizada por aparelho de escaneamento de lâminas. A imunoexpressão foi avaliada pelo percentual de células coradas e foram obtidos escores de intensidade. Foram considerados como positivos para CD 10 os tumores que expressavam o marcador em mais de 10% das células neoplásicas. Para NM 23 considerou-se dois grupos divididos em fortes expressores (mais de 50%) e expressores fracos (menos de 50%) das células coradas. Os resultados foram relacionados com as características morfológicas e histopatológicas do carcinoma colorretal, estadiamento clínico, presença de metástases hepáticas e com o prognóstico. No estudo estatístico foram utilizados os testes de Mann-Whitney, Kruskal- Wallis e exato de Fisher. A sobrevivência foi avaliada utilizando a curva de Kaplan- Meier, e o desfecho de comparação entre as curvas foi calculado pelo teste de Long rank. Resultados: Ambos os marcadores CD10 e NM23 apresentaram expressão maior no tecido do carcinoma do que na mucosa não neoplásica adjacente (p<0,0001 para ambos). A imunoexpressão tecidual das proteínas NM23 e CD10 não apresentou relação com o grau de diferenciação celular (p=0,57 e p=0,48, respectivamente), invasão vascular (p=0,85 e p=0,67, respectivamente), invasão linfática (p=0,41 e 0,73, respectivamente), infiltração perineural (p=0,46 e p=0,24, respectivamente) e com o estadiamento pela classificação TNM (p=0,19 para ambos). A imunoexpressão de CD10 no tecido do carcinoma colorretal foi maior (p=0,05) nas neoplasias exofíticas do que nos tumores não exofíticos. A expressão das proteínas NM23 e CD10 não apresentou relação com a incidência de metástases linfonodais (p=0,08 e 0,30, respectivamente). A expressão tecidual dos marcadores NM23 e CD10 não se relacionou com a ocorrência de metástases hepáticas (p=0,59 e p=0,31, respectivamente). A sobrevivência livre de doença mostrou relação significante (p=0,01) com a maior intensidade de imunoexpressão da proteína NM23 no tecido do carcinoma colorretal, o mesmo não ocorrendo com a imunoexpressão da proteína CD10 (p=0,18). A sobrevivência global não mostrou relação com as expressões das proteínas NM23 e CD10 (p=0,13 e p=0,24, respectivamente). Conclusões: O tecido neoplásico do carcinoma colorretal expressou mais intensamente as proteínas NM23 e CD10 do que a mucosa não neoplásica adjacente. A imunoexpressão de CD10 no tecido do carcinoma colorretal foi maior (p=0,05) nas neoplasias exofíticas do que nos tumores não exofíticos. A expressão das proteínas NM23 e CD10 não se relacionou com os demais aspectos anatomopatológicos da neoplasia, com a presença de metástase hepática e com o estadiamento do carcinoma colorretal. Os doentes com imunoexpressão aumentada da proteína NM23 apresentaram sobrevivência livre de doença significativamente maior. A intensidade da imunoexpressão tecidual da proteína CD10 não influenciou a sobrevivência livre de doença e a sobrevivência global não se relacionou com a imunoexpressão das proteínas NM23 e CD10.
Aims: To analyze the tissue expression of the proteins CD 10 and NM 23 through the immunohistochemichal study of the colorectal carcinoma and evaluate the expression relation of these proteins with the anatomopathological aspects of the neoplasia, clinical staging, occurrence of hepatic metastasis and patients’ prognostic. Method: One hundred and thirty operated patients of colorectal carcinoma have been analyzed. A block of tissue microarray was produced with the neoplastic mucosa and with the adjacent non-neoplastic mucosa. An immunohistochemichal study was performed with monoclonal antibodies NM23 and CD10 on the neoplastic tissue and non-neoplastic tissue of the adjacent mucosa. The interpretation of the slides was made by a scanner device. The immunoexpression was evaluated by the percentage of colored cells and the obtained intensity scores. The results were related to the morphological and histopathological characteristics of the carcinoma, clinical staging, presence of hepatic metastasis and to the prognostic of the patients. In the statistic study were used the Mann-Whitney test, the Kruskal-Wallis test and Fisher’s exact test. The analysis of survival was conducted with the use of the Kaplan-Meier curve and the comparison conclusion between the curves was calculated through the Longrank test. Results: Both markers CD10 and NM23 presented a higher expression on the carcinoma tissue rather than on the non-neoplastic adjacent mucosa (p<0,0001 for both). The expression of the proteins NM23 and CD10 did not present any relation to the degree of cellular differentiation (p=0,57 and p=0,48, respectively) , vascular invasion (p=0,85 and p=0,67, respectively), lymphatic invasion (p=0,41and 0,73, respectively), perineural infiltration (p=0,46 and p=0,24, respectively) and with the staging by the TNM classification (p=0,19). The immunoexpression of CD10 on the colorectal carcinoma tissue was higher (p=0,15) on the exophytic neoplasias than on the non-exophytic tumors. The expression of the proteins NM23 and CD10 did not present any relation with the incidence of lymphonodal metastasis (p=0,08 and 0,30, respectively). The tissue expression of the markers NM23 and CD10 did not relate to the occurrence of hepatic metastasis (p=0,59 and 0,31 respectively). The disease-free survival disclosed a significant relation (p=0,01) with a higher intensity of immunoexpression of the protein NM23 on the colorectal carcinoma’s tissue. However, the same did not occur with the immunoexpression of the protein CD10 (p=0,18). The global survival did not show any relation with the expression of the proteins NM23 and CD10 (p=0,13 and p=0,24, respectively). Conclusions: The neoplastic tissue of the colorectal carcinoma expresses more intensely the proteins NM23 and CD10 than the adjacent nonneoplastic mucosa. The expression of the proteins NM23 and CD10 does not relate to the presence of lymphonodal metastasis, hepatic metastasis, degree of cellular differentiation, colonic or rectal localization of the neoplasia, presence of vascular and/or lymphatic invasion, presence of neural infiltration and the staging of the colorectal carcinoma. The patients with increased immunoexpression of the protein NM23 presented a disease-free survival significantly higher. The intensity of the tissue immunoexpression of the protein CD10 did not influence the disease-free survival. The global survival does not relate to the immunoexpression of the proteins NM23 and CD10.
TEDE
BV UNIFESP: Teses e dissertações

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Fernandez, Sonia. „CD4? T-cell deficiency and dysfunction in HIV patients receiving combination antiretroviral therapy“. University of Western Australia. School of Surgery and Pathology, 2007. http://theses.library.uwa.edu.au/adt-WU2007.0120.

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[Truncated abstract] Failure to fully reconstitute the immune system is a common clinical problem in HIV patients who were severely immunodeficient before responding to combination antiretroviral therapy (CART). This can manifest as a deficiency in the number or function of CD4+ T-cells and occurs most often in patients who had a nadir CD4+ T-cell count below 100/μl when CART was commenced. Observational studies of large cohorts of HIV patients, such as the D:A:D study, have demonstrated that patients with low CD4+ T-cell counts have increased rates of death compared with patients who have normal CD4+ T-cell counts. Furthermore, individual case studies suggest that impaired recovery of pathogen-specific immune responses during CART is associated with opportunistic infections or disease progression. This thesis addresses possible causes of deficiencies in CD4+ T-cell number or function in HIV patients who were very immunodeficient prior to treatment and are responding (virologically) to CART. Firstly, the role of the thymus in producing naive CD4+ T-cells and the effects of persistent immune activation on the recovery of CD4+ T-cell numbers were assessed in patients with either low or high CD4+ T-cell counts after long-term CART. ... Proportions of antigen presenting cell (APC) subpopulations were examined in HIV patients with low or high CMV-specific CD4+ T-cell responses after long-term CART. HIV patients had significantly lower proportions of plasmacytoid dendritic cells (pDC) than HIV-negative controls. Furthermore, the proportions of pDC were positively correlated with CMV-specific CD4+ T-cell responses in HIV patients. Proportions of myeloid dendritic cells (mDC) were significantly higher in HIV patients than controls, and were also increased in patients with low CMV-specific CD4+ T-cell responses. Proportions of M-DC8+ dendritic cells or CD14+ monocytes did not differ between patients and controls, nor were they associated with CMV-specific CD4+ T-cell responses. Quantitation of cytokine (interferon-α, tumour necrosis factor-α, interleukin (IL) -12, IL-23, IL-15, IL-18 and IL-10) mRNA in unstimulated, purified populations of the APC described above revealed few significant differences between patients with low or high CD4+ T-cell IFN-γ responses to CMV. The only notable difference was the slight elevation of IL-15 mRNA levels in patients compared to controls. Since patients in the high responder group had the highest levels of IL-15 mRNA, this association may reflect the anti-apoptotic properties of IL-15. These studies provide valuable insights into the causes of persistent CD4+ T-cell deficiency and dysfunction in HIV patients on CART and may lead to better monitoring and treatments.

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