Dissertations / Theses: 'Cell surface antigen receptors'

1

Mallett, Susan. "Characterization of T lymphocyte antigens." Thesis, University of Oxford, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.293461.

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2

Deftos, Michael Laing. "Notch signaling in T cell development /." Thesis, Connect to this title online; UW restricted, 2001. http://hdl.handle.net/1773/8364.

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3

Gadd, Stephen J. "Analysis of acute mycloid leukaemia cell surface antigens with monoclonal antibodies." Title page, contents and abstract only, 1985. http://web4.library.adelaide.edu.au/theses/09PH/09phg123.pdf.

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4

Watanabe, Norihiko. "Antigen receptor cross-linking by anti-immunoglobulin antibodies coupled to cell surface membrane induces rapid apoptosis of normal spleen B cells." Kyoto University, 1998. http://hdl.handle.net/2433/182246.

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5

Gray, Daniel Herbert Donald. "Thymic stromal cells : population dynamics and their role in thymopoiesis." Monash University, Dept. of Pathology and Immunity, 2003. http://arrow.monash.edu.au/hdl/1959.1/9409.

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6

Clarke, Raedun Laurie. "The signal transduction pathways initiated by CD8 during apoptosis of thymocytes /." Connect to full text via ProQuest. Limited to UCD Anschutz Medical Campus, 2007.

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Thesis (Ph.D. in Immunology) -- University of Colorado Denver, 2007.
Typescript. Includes bibliographical references (leaves 236-251). Free to UCD affiliates. Online version available via ProQuest Digital Dissertations;

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7

Alheim, Mats. "Inhibitory receptors of natural killer cells : specificity and regulation /." Stockholm, 1998. http://diss.kib.ki.se/search/diss.se.cfm?19981009alhe.

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8

Leprince, Corinne. "Regulation de la fonction des lymphocytes b humains : interactions entre proteines membranaires et facteurs solubles." Paris 6, 1988. http://www.theses.fr/1988PA066361.

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Etude de la regulation de la reponse immune due aux lymphocytes b a travers leur sensibilite a des signaux regulateurs solubles (interleukines et facteurs bcgf) et l'expression de deux molecules de surface, les antigenes cd5 et b8. 7

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9

Hauser, Jannek. "Regulation of B cell development by antigen receptors." Doctoral thesis, Umeå universitet, Institutionen för molekylärbiologi (Medicinska fakulteten), 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-40819.

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The developmental processes of lymphopoiesis generate mature B lymphocytes from hematopoietic stem cells through increasingly restricted intermediates. Networks of transcription factors regulate these cell fate choices and are composed of both ubiquitously expressed and B lineage-specific factors. E-protein transcription factors are encoded by the three genes E2A, E2-2 (SEF2-1), and HEB. The E2A gene is required for B cell development and encodes the alternatively spliced proteins E12 and E47. During B lymphocyte development, the cells have to pass several checkpoints verifying the functionality of their antigen receptors. Early in the development, the expression of a pre-B cell receptor (pre-BCR) with membrane-bound immunoglobulin (Ig) heavy chain protein associated with surrogate light chain (SLC) proteins is a critical checkpoint that monitors for functional Ig heavy chain rearrangement. Signaling from the pre-BCR induces survival and a limited clonal expansion. Here it is shown that pre-BCR signaling rapidly down-regulates the SLCs l5 and VpreB and also the co-receptor CD19. Ca2+ signaling and E2A were shown to be essential for this regulation. E2A mutated in its binding site for the Ca2+ sensor protein calmodulin (CaM), and thus with CaM-resistant DNA binding, makes l5, VpreB and CD19 expression resistant to the inhibition following pre-BCR stimulation. Thus, Ca2+ down-regulates SLC and CD19 gene expression upon pre-BCR stimulation through inhibition of E2A by Ca2+/CaM. A general negative feedback regulation of the pre-BCR proteins as well as many co-receptors and proteins in signal pathways from the receptor was also shown. After the ordered recombination of Ig heavy chain gene segments, also Ig light chain gene segments are recombined together to create antibody diversity. The recombinations are orchestrated by the recombination activating gene (RAG) enzymes, other enzymes that cleave/mutate/assemble DNA of the Ig loci, and the transcription factor Pax5. A key feature of the immune system is the concept that one lymphocyte has only one antigen specificity that can be selected for or against. This requires that only one of the alleles of genes for Ig chains is made functional. The mechanism of this allelic exclusion has however been an enigma. Here pre-BCR signaling was shown to down-regulate several components of the recombination machinery including RAG1 and RAG2 through CaM inhibition of E2A. Furthermore, E2A, Pax5 and the RAGs were shown to be in a complex bound to key sequences on the IgH gene before pre-BCR stimulation and instead bound to CaM after this stimulation. Thus, the recombination complex is directly released through CaM inhibition of E2A. Upon encountering antigens, B cells must adapt to produce a highly specific and potent antibody response. Somatic hypermutation (SH), which introduces point mutations in the variable regions of Ig genes, can increase the affinity for antigen, and antibody effector functions can be altered by class switch recombination (CSR), which changes the expressed constant region exons. Activation-induced cytidine deaminase (AID) is the mutagenic antibody diversification enzyme that is essential for both SH and CSR. The AID enzyme has to be tightly controlled as it is a powerful mutagen. BCR signaling, which signals that good antibody affinity has been reached, was shown to inhibit AID gene expression through CaM inhibition of E2A. SH increases the antigen binding strength by many orders of magnitude. Each round of SH leads to one or a few mutations, followed by selection for increased affinity. Thus, BCR signaling has to enable selection for successive improvements in antibodies (Ab) over an extremely broad range of affinities. Here the BCR is shown to be subject to general negative feedback regulation of the receptor proteins as well as many co-receptors and proteins in signal pathways from the receptor. Thus, the BCR can down-regulate itself to enable sensitive detection of successive improvements in antigen affinity. Furthermore, the feedback inhibition of the BCR signalosome and most of its protein, and most other gene regulations by BCR stimulation, is through inhibition of E2A by Ca2+/CaM. Differentiation to Ab-secreting plasmablasts and plasma cells is antigen-driven. The interaction of antigen with the membrane-bound Ab of the BCR is critical in determining which clones enter the plasma cell response. Genome-wide analysis showed that differentiation of B cells to Ab-secreting cell is induced by BCR stimulation through very fast regulatory events, and induction of IRF-4 and down-regulation of Pax5, Bcl-6, MITF, Ets-1, Fli-1 and Spi-B gene expressions were identified as immediate early events. Ca2+ signaling through CaM inhibition of E2A was essential for these rapid down-regulations of immediate early genes after BCR stimulation in initiation of plasma cell differentiation.

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10

Wilson, Keith Michael. "Single particle fluorescent imaging analysis of cell surface HLA-DR and associated CD74 antigens." Thesis, University of Essex, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.361022.

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11

Hannan, S. B. "Cell surface mobility of GABAB receptors." Thesis, University College London (University of London), 2011. http://discovery.ucl.ac.uk/1335825/.

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Type-B γ-aminobutyric acid receptors (GABABRs) are important for mediating slow inhibition in the central nervous system and the kinetics of their internalisation and lateral mobility will be a major determinant of their signalling efficacy. Functional GABABRs require R1 and R2 subunit co-assembly, but how heterodimerisation affects the trafficking kinetics of GABABRs is unknown. Here, an α-bungarotoxin binding site (BBS) was inserted into the N-terminus of R2 to monitor receptor mobility in live cells. GABABRs are internalised via clathrin- and dynamin-dependent pathways and recruited to endosomes. By mutating the BBS, a new technique was developed to differentially track R1a and R2 simultaneously, revealing the subunits internalise as heteromers and that R2 dominantly-affects constitutive internalisation of GABABRs. Notably, the internalisation profile of R1aR2 heteromers, but not R1a homomers devoid of their ER retention motif (R1ASA), is similar to R2 homomers in heterologous systems. The internalisation of R1aASA was slowed to that of R2 by mutating a di-leucine motif in the R1 C-terminus, indicating a new role for heterodimerisation, whereby R2 subunits slow the internalization of surface GABABRs. R1a and R1b are the predominant GABABR1 isoforms in the brain, differing by the two Sushi Domains (SDs) in R1a. Introduction of a BBS into the N-terminus of R1b and comparison with R1a revealed that R1bR2 internalises faster than R1aR2. Introduction of the SDs into the BBS-tagged metabotropic glutamate receptor-2 also conferred a decrease in internalisation. Finally, the lateral surface mobility of GABABRs was studied by extending the BBS-tagging method to single-particle tracking using quantum dots. R1aR2 and R1bR2 exhibited different mobility profiles on hippocampal neurons and differentially responded to baclofen. In conclusion, this study provides new and important insight into the mobility of cell surface GABABRs and the underlying mechanisms that ensure they provide efficacious slow synaptic inhibition.

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12

Dubois, Patrice. "Signal transduction by the surface antigen receptors of B lymphocytes." Doctoral thesis, Universite Libre de Bruxelles, 1991. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/213058.

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13

Page, Theresa Helen. "Studies of rat cell surface activation antigens : molecular characterisation of the alpha and beta chains of the interleukin-2 receptor." Thesis, University of Oxford, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.280535.

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14

Pesce, John Thomas. "Early events leading to the host protective Th2 immune response to an intestinal nematode parasite /." Download the dissertation in PDF, 2005. http://www.lrc.usuhs.mil/dissertations/pdf/Pesce2005.pdf.

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15

Border, Ellen Clare. "Structural and functional studies of cell surface receptors." Thesis, University of Oxford, 2012. http://ora.ox.ac.uk/objects/uuid:907793da-3ba1-4a57-8bdb-c185aa84c28c.

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Receptor proteins on the surfaces of cells equip them to communicate with each other and to sense and interact with their environment. One receptor family, the αβ T-cell receptors (TCRs), allow T lymphocytes to detect and respond to pathogens via interactions with antigen-presenting major histocompatibility complex (MHC) molecules on target cells. A degree of TCR cross-reactivity (e.g. through structural similarity between peptide-MHC (pMHC) complexes) is essential to account for all possible pathogens, but can also lead to the misinterpretation of self antigens as foreign, and thereby elicit an autoimmune response, resulting in diseases such as multiple sclerosis (MS). Structural studies of pMHC and TCR-pMHC complexes have been key to developing of an understanding of the molecular basis of TCR cross reactivity, and the first strand of this thesis describes attempts to express and purify a highly cross-reactive MS patient-derived TCR for structural characterisation. The formation, purification and crystallisation of a TCR-self pMHC complex including another autoreactive TCR is also described. Another family of receptors, the fibronectin leucine-rich transmembrane proteins (FLRTs), has been implicated in roles in embryonic development including cell sorting and adhesion. In the second strand of this thesis, the nature of homotypic interactions between FLRTs, which may underlie adhesion between FLRT transfected cells, is investigated. Biophysical analyses demonstrate that these interactions may be mediated by the extracellular leucine-rich repeat (LRR) domain, and crystal structures of all three FLRT LRR domains suggest how interactions between them may underlie FLRT self-association at the cell surface. Residues which contribute to these interactions are conserved across different members of the FLRT family and different species. These findings confirm that FLRTs induce homotypic cell-cell adhesion, and suggest that this behaviour is mediated by self association at the cell surface via the LRR domain.

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16

Yuan, Fang. "Cell Surface Recognitions by Viral and Immune Receptors." Thesis, University of Oxford, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.491598.

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Cell surface recognition is an important interaction occurring between proteins on opposite cell surfaces and transmits signals that allow cells to adapt to their environment. Viruses utilise recognition for entering host cells, and the immune system may defend against numerous attacks from environment through these interactions, by generating a protective adaptive immune response. This thesis offers insight into cell surface recognition through both viral and immune system molecules. For virus research, West Nile virus receptor binding domain was refolded and crystallized. Structural information ofthis domain was obtained and analysed. A putative receptor binding loop was identified from the structure. For immune research, T cell receptors that recognized Melan-A peptide, ELAGIGILTV, and gplOO peptide, YLEPGPVTV, were identified from several CD8+ T cell clones. Kinetic studies of these TCRs were carried out against rel<\ted human peptide-major histocompatibility complex by using surface plasmon resonance techniques. One ofthese TCRs which recognize Melan-A peptide was successfully crystallized with its ligand peptide-major histocompatibility complex. .J i Structural information obtained from X-ray diffraction studies ofviral and immune molecules indicated that protein-protein interactions are often effected by disordered/flexible regions in protein structures. For viruses, this flexible region is the binding loop and for T cell r.eceptors it is the complementarity determining regions. Such conformational flexibility allows specific protein interactions distinguishing small differences in amino acid composition. Alteration ofthe flexible regions of virus could be a potential mechanism to prevent cell entry and similarly, alteration of complementarity determining regions ofT cell receptors could lead to higher affmity for its ligand, major histocompatibility complex.

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17

Gosselin, Edmund J. "Characterization of Antigen-Specific Antigen Processing by the Resting B cell: a Thesis." eScholarship@UMMS, 1988. https://escholarship.umassmed.edu/gsbs_diss/199.

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An optimal antibody response to a thymus-dependent antigen requires cooperation between the B cell and an antigen-specific helper T cell. Major histocompatibility complex restriction of this interaction implies that the helper T cell recognizes antigen on the B cell surface in the context of MHC molecules, and that the antigen-specific B cell gets help by acting as an antigen presenting cell for the helper T cell. However, a number of studies have shown that normal resting B cells are ineffective as antigen presenting cells, implying that the B cell must leave the resting state before it can interact specifically with a helper T cell. On the contrary, other studies, including those using rabbit Ig as antigen, and rabbit globulin-specific mouse T cell lines and hybridomas, show that certain T cell lines can be efficiently stimulated by normal resting B cells. One possibility I considered was that small B cells are unable to process antigens, and that the rabbit Ig-specific T cell lines used above recognize native antigen on the B cell surface. In the majority of cases, experiments with B cell lines and macrophages have shown that antigen presentation requires antigen processing, a sequence of events which includes: internalization of antigen into an acid compartment, denaturation or digestion of antigen into fragments, and the return of processed antigen to the cell surface where it can then be recognized by the T cell in the context of class II molecules of the MHC. The experiments reported here show that the rabbit Ig-specific T cell lines do require an antigen processing step, and that small resting B cells, like other antigen presenting cells, process antigen before presenting it to T cells. Specifically, I show that an incubation of 2-8 hours is required after the antigen pulse before antigen presentation becomes resistant to fixation or irradiation. Shortly after the pulse, the antigen enters a pronase resistant compartment. Chloroquine, which raises the pH of endocytic vesicles, inhibits presentation. In addition, a large excess of antibody to native antigen fails to block presentation of antigen after a 2-8 hour incubation. Also, although membrane Ig, the antigen receptor on the B cell, is required for efficient presentation of antigen at low concentrations, antigen is no longer associated with the B cell receptor at the time of presentation to the T cell. Modulation of membrane Ig by anti-Ig blocks presentation before but not after the antigen pulse.

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18

Brown, Marion Hanbury. "Physical interactions of the CD2 antigen." Thesis, Open University, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.277634.

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19

Murray, Fiona. "Stereotyped B Cell Receptors in Chronic Lymphocytic Leukaemia : Implications for Antigen Selection in Leukemogenesis." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Universitetsbiblioteket [distribution], 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-9438.

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20

Simmons, Daimon P. "Effects of Toll-Like Receptors and Type I Interferon on Dendritic Cell Maturation and Activation of T Cells." Case Western Reserve University School of Graduate Studies / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=case1311278278.

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21

Bas, Anna. "Extrathymic T cell receptor gene rearrangement in human alimentary tract /." Umeå : Univ, 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-169.

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22

Hu, Jiancheng. "Regulation of Lsc activity and role in B cell migration and antigen receptor signaling /." Connect to full text via ProQuest. Limited to UCD Anschutz Medical Campus, 2007.

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Thesis (Ph.D. in Immunology) -- University of Colorado Denver, 2007.
Typescript. Includes bibliographical references (leaves 103-118). Free to UCD affiliates. Online version available via ProQuest Digital Dissertations;

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23

Forni, Luciana. "Recepteurs membrananires des lymphocytes b : interactions entre recepteurs et physiologie des cellules b." Paris 6, 1987. http://www.theses.fr/1987PA066375.

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24

Parra, Eduardo. "Molecular basis for costimulation of human T lymphocytes." Lund : Lund University, 1998. http://books.google.com/books?id=SgFrAAAAMAAJ.

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25

Lee, Edwin A. M. "T-cell responses to Plasmodium falciparum merozoite surface protein-1." Thesis, University of Oxford, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.325150.

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26

Wong, Phillip. "Changing TCR recognition requirements at discrete stages of intrathymic CD4 T cell development /." Thesis, Connect to this title online; UW restricted, 2000. http://hdl.handle.net/1773/8351.

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27

Jacobs, Caron Adrienne. "The nanoscale organisation of HIV cell surface receptors CD4 and CCR5." Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10056281/.

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The plasma membrane serves as the cell’s front line for interactions with, and response to, the external environment. The molecular mechanisms and regulation of cellular responses to extracellular signals are determined by the spatial organisation and dynamics of the various components comprising the plasma membrane. CD4 and CCR5 are two key cell surface molecules with important roles in immune cell function and regulation. They are also co-opted as the primary receptor and a co-receptor, respectively, by HIV. Biochemical studies have provided a detailed understanding of the molecular mechanisms of these interactions. Until recently, however, the small scale and rapid dynamics of these interactions has meant that a detailed view of the topology of the cell membrane and the organisation of receptors first encountered by the virus has been beyond the resolving power of available tools. The increasing capabilities of the emerging and rapidly developing super-resolution microscopy technologies are now optimally poised for us to address some of these questions. In this work, I have applied single molecule localization microscopy to unveil some of the nanoscale organisational properties of the cell surface receptors CD4 and CCR5. I have worked on the development of small labelling probes for CD4 and addressed some of the key aspects of sample preparation and labelling that can artificially alter the distribution of membrane associated target molecules. Here I report the first quantitative characterisation of the nanoscale organisation of CD4 and CCR5 in lymphoid cell plasma membranes, as well as how this organisation changes under different conditions, such as in response to cell signal-mimicking stimulation, or exposure to HIV envelope. This approach to characterising membrane receptor organisation can be further applied to in-depth studies of early host cell-virus interactions, as well as to other cell surface receptors and their organisation in the context of key cellular functions.

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28

Jin, Ming-Jie. "Intracellular transport pathway of cell surface receptors to the Golgi complex." Case Western Reserve University School of Graduate Studies / OhioLINK, 1990. http://rave.ohiolink.edu/etdc/view?acc_num=case1054916831.

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29

Kwong, Pearl Chu. "Characterization of an antigen-specific T helper cell clone and its products." Thesis, University of British Columbia, 1987. http://hdl.handle.net/2429/27366.

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A T helper cell clone, referred to as clone 9, was derived from an allogeneic mixed lymphocyte culture. Clone 9, as well as supernatant factor(s) derived from it, could help the cytotoxic T lymphocyte (CTL) responses of H-2 Db (Db) responder cells to alloantigens, or they could help the CTL responses of non- Db responder cells to Db alloantigens. Clone 9 cells or their factor(s) were active only when added during the first 24 hours of a five-day culture period. Clone 9 or its factor(s) could also synergize with interleukin-2 (IL-2)-containing medium in mounting cytotoxic responses to alloantigens. The helper activity in clone 9 supernatant was not due to IL-2 and it was specifically absorbed out by Db -spleen cells. The characterization of the Db -specific helper factor(ASHF) was facilitated by the isolation of a T hybridoma clone (clone 25), obtained from fusion of clone 9 cells with the T cell lymphoma, BW5147, and a B cell hybridoma that produced an IgM monoclonal antibody (clone 30 IgM) which bound ASHF. An additional monoclonal antibody (F23.1), which recognizes a determinant of the Vβ8 family of the T cell receptor, was also particularly useful for the characterization of ASHF. Analysis with these reagents showed that both clone 30 IgM and F23.1 immunoadsorbents could retain ASHF activity. Preabsorption of the ASHF with Db spleen cells prior to affinity purification over a clone 30 IgM column resulted in the absorption of Db-specific helper activity as well as the loss of a 50,000 molecular weight (MW) band on SDS-PAGE under reducing conditions. Furthermore, affinity purification of ASHF over the F23.1 immunoadsorbent, but not an irrelevant monoclonal antibody (mAb) column, also yielded a 50,000 MW molecule. Taken together, these findings suggest that the 50,000 MW molecule is a component of the ASHF and it is intimately related to the B chain of the T-cell receptor. The mode of action of clone 9 and its products in the induction bfCTL responses was also investigated. It was found that clone 9 and ASHF could help CTL responses by inducing IL-2 production in B6-stimulated cultures. In addition to ASHF, clone 9 cells also produced an additional factor(s) which participated in the induction of CTL responses. This additional factor(s) was referred to as IL-X. IL-X synergized with excess human recombinant IL-2 in the activation of CTL precursors (CTL-P) in the absence of antigenic stimulation. A model which involves the participation of ASHF, T helper cells, IL-2 and IL-X in the induction of CTL responses is proposed.
Science, Faculty of
Microbiology and Immunology, Department of
Graduate

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30

Giusti, Pablo. "Characterization of antigen-presenting cell function in vitro and ex vivo." Doctoral thesis, Stockholms universitet, Wenner-Grens institut, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-60433.

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Long-term protective immunity depends on proper initiation of professional antigen-presenting cells (APCs). Autoimmune disorders and certain infections can cause disease through modulation of APCs and thereby affecting the outcome of these diseases. This work aimed to investigate the behaviour of different APC subsets during conditions known to cause improper immune responses. In Paper I, the effects of an anti-inflammatory compound called Rabeximod, intended for treatment of rheumatoid arthritis were investigated on different subsets of APCs. The results showed that Rabeximod affected the differentiation and behaviour of inflammatory subsets of dendritic cells (DCs) and macrophages while no effects were observed on anti-inflammatory subsets. Our findings suggest that Rabeximod acts by inhibiting the functionality of inflammatory subsets of APCs. In Paper II, the effects of different malaria derived stimuli such as hemozoin (Hz) and infected red-blood cells (iRBCs) on monocyte-derived dendritic cells (MoDCs) were investigated. Both stimuli triggered activation and migration of MoDCs. MoDCs exposed to iRBCs induced allogeneic T-cell proliferation while those exposed to Hz did not. These results indicate that different malaria derived stimuli may differently affect DCs and that this could lead to improper and inefficient T-cell activation. In Paper III, innate aspects of malarial immunity were compared in children from two sympatric ethnic groups. We observed decreased activation of APCs and severely supressed TLR responses in Dogon children as compared to Fulani. This may indicate an important role for TLR and APC activation in the Fulani, known to be better protected against malaria than the Dogon. In summary, detailed knowledge of APC activation will be helpful in the understanding of specific effector immune responses. This could in turn, improve treatment of inflammatory disorders as well as the generation of efficient vaccines against infectious diseases.

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Nibber, Anjan. "Antibodies directed against AMPA and GABAB receptors in neurological diseases and identification of novel antigen targets." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:5d3eb5fa-9f51-4415-92bd-2d7c795aa51c.

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Antibodies directed against AMPAR and GABA_BR subunits have been implicated in forms of limbic encephalitis (LE), a disease characterised by memory loss and seizures. Patients with LE show clinical improvement with immunomodulatory treatment, suggesting that the associated antibodies are pathogenic. To explore further the AMPAR and GABA_BR antibodies, an in house cell based assay (CBA) was established for screening and potential pathogenicity was explored using a series of in vitro experiments. Human embryonic kidney (HEK) cells transfected with AMPAR and GABA_BR subunits and primary neuronal cultures were used to detect antibodies in patient sera and CSF. In total, 15/1361 (1.1%) AMPAR antibody positive samples and 24/1438 (1.7%) GABABR antibody positive samples were identified. The predominant antibody subclass for AMPAR and GABA_BR antibodies was shown to be IgG1. Interestingly, on transfected cells, only AMPAR antibodies showed complement deposition, and therefore had the potential to activate the classical pathway of the complement cascade. Application of IgG purified from AMPAR antibody positive patients, but not GABA_BR antibody positive patients caused a down regulation of the receptor from the cell surface of transfected HEK cells and primary hippocampal cultures. Electrophysiological analysis showed changes in Up state duration and spike rate in the entorhinal cortex following application of purified GABA_BR antibody IgG on brain slices. These findings suggest that GABABR antibodies are having a direct short term effect on GABA_BRs, and by extension cortical networks. Finally, we attempted to study whether or not viral infection could be a trigger for antibody production to known and novel antigen targets in a cohort of Japanese encephalitis viral (JEV) samples. A JEV cohort of 44 children was screened for antibodies to neuronal surface proteins by CBA. Twenty-seven percent of patients had antibodies to known neuronal surface antigens, with NMDAR and CASPR2 as the most common antigen targets. Interestingly, screening the cohort on primary neuronal cultures revealed that 65.9% of children with JEV have neuronal surface antibodies. The identification of the novel antigen target was attempted using immunoprecipitation and mass spectrometry techniques. In total, 4 neuronal surface proteins were identified that could be potential targets in JEV patients. In summary, antibodies directed against previously described antigenic targets were explored further for pathogenic potential, and a cohort of patients with a viral infection with potential novel antigen targets was investigated.

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32

Labastide, Wayne Brian. "Characterisation of a novel lymphocyte surface antigen associated with cutaneous T-cell lymphoma." Thesis, University of Cambridge, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.385436.

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33

Thomas, Elaine Rhiannon. "Neutralisation of HIV-2 interactions between viral glycoproteins and cell surface receptors." Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.397817.

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34

Levander, Louise. "Effects of α1‐acid glycoprotein onpolymorphonuclear leukocytes ‐involvement of cell surface receptors." Doctoral thesis, Linköpings universitet, Cellbiologi, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-20271.

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Alpha1‐acid glycoprotein (AGP) is a highly glycosylated lipid‐binding acute‐phaseprotein. Although the exact mechanisms are unknown, several studies havesuggested that AGP may regulate the function of neutrophils and hence modulateinflammatory responses. The general aim of this thesis was to investigate if AGP isable to mediate intracellular signalling in neutrophils through binding to specificreceptors. Measurements of intracellular calcium concentration showed that AGP elicited asmall rise in [Ca2+]i in neutrophils that was markedly enhanced by pre‐treatmentwith anti‐L‐selectin antibodies. In contrast, desialylation of AGP reduced the Ca2+mobilizing capacity significantly. The AGP‐induced Ca2+ signal was mediatedthrough Src tyrosine kinases, PLC and PI3K which suggests involvement of cellsurface receptors. Indeed, AGP was shown to bind to, and mediate Ca2+ signallingthrough, sialic acid binding immunoglobulin‐like lectin (Siglec)‐5 and/or ‐14.Increased fucosylation of AGP is common during acute‐phase reactions. We showthat hyperfucosylated AGP has a diminished Ca2+ signalling capacity compared tonormally fucosylated AGP. This could be due to a reduced capacity of AGP tointeract with Siglec‐5/‐14 since it is known that the presence of fucose residues onsialylated glycans has a negative effect on Siglec‐5/‐14 affinity. AGP was alsodemonstrated to bind to the neutrophil proteins S100A8 and S100A9. In additionwe show that AGP‐bound hydroxyeicasotetraenoic acids (HETEs) induce increasesin [Ca2+]i in neutrophils through binding to the leukotriene B4 receptor BLT2. Wepropose a two‐step binding model where AGP binds to Siglec‐5/‐14 on L‐selectinactivated neutrophils. This may orient AGP in a way that assists an interactionbetween AGP and the neutrophil membrane which favours transfer of AGP‐boundHETEs to the BLT2 receptor. In conclusion, these data gives new insights regarding how AGP interacts with andmediates signalling in human neutrophils and supports the view of AGP as beingan acute phase reactant with immunomodulatory properties.

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35

Chan, Po-Ying. "Characterization and cDNA cloning of a novel murine T cell surface antigen YE1/48." Thesis, University of British Columbia, 1988. http://hdl.handle.net/2429/28640.

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T cell surface antigens are thought to play significant roles in immunological functions. They are involved in cellular interactions and T cell activation and proliferation. Characterization of T cell antigens is important in understanding the molecular machanisms underlying immune responses. The subject of this thesis is to characterize a novel murine T cell surface antigen called YE1/48. YE1/48, defined by two rat monoclonal antibodies YE1/48.10.6 and YE1/32.8.5, is a dimeric glycoprotein with molecular size and charge resembling the murine T cell antigen receptor α/β. It was initially detected at high levels on two T cell lymphomas, EL-4 and MBL-2. In my thesis studies, the YE1/48 antigen was characterized biochemically, a cDNA clone was isolated, and its expression in lymphoid cell populations was determined. The YE1/48 antigen was found to be distinct from the T cell receptor based on direct comparisons of their primary sequences as well as immunological analyses. It is likely a homodimer with similar or identical subunits. No homology with any known proteins could be detected, including the human T cell activation antigen CD28 (T44) which also has a similar dimeric structure as YE1/48. No function of the YE1/48 antigen could be derived from its primary sequence or with the use of the two monoclonal antibodies because the antibodies do not appear to bind to the surface of intact normal T lymphocytes. Some intriguing characteristics of the YE1/48 antigen were observed in the current studies. The YE1/48 antigen belongs to a rare group of type II membrane proteins with orientation of the amino-terminus inside the cell and the carboxy-terminus outside. The YE1/48 gene may have two alleles among different mouse strains and may belong to a multigene family. YE1/48 is expressed at low levels on a wide range of T cells with no restriction to their differentiation stages, and on spleen B cells as well as bone marrow cells. Its expression on lymphocytes is not related to activation or proliferation. However, YE1/48 expression appears to be induced at high levels by Abelson Murine Leukemia Virus-transformation of pre-B cells. Moreover, the epitopes defined by the YE1/48.10.6 and YE1.32.8.5 antibodies seem to be exposed only on three T lymphomas but not on normal T cells. It is thus tantalizing to speculate a correlation of the high level expression of YE1/48 antigen and its epitope exposure on transformed lymphocytes with cellular transformation. In summary, YE1/48 was found to be a novel T cell surface antigen which has similar dimeric structure as the murine T cell receptor α/β and human CD28 (T44). It has now been characterized biochemically, molecularly cloned, and its expression on lymphoid cells has been determined. Although the function of YE1/48 antigen remains unknown, a number of intriguing characteristics observed in the current studies have certainly called for further studies on the antigen and the determination of its function.
Science, Faculty of
Microbiology and Immunology, Department of
Graduate

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36

Hayashi, Fumitaka. "The characterization of TLR5 /." Thesis, Connect to this title online; UW restricted, 2001. http://hdl.handle.net/1773/8330.

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37

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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38

Adamson, Janet. "Structure and function of the platelet and T-cell activation antigen-1 (PTA1)." Thesis, University of Liverpool, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.367096.

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39

Cowan, Teresa. "The TCRBJ and TCRBV repertoire in naive and memory human T-cells." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ34173.pdf.

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40

Yuan, Xiaohui. "Characterization of the ligand-binding specificity and transcriptional properties of estrogen receptor homodimeric/heterodimeric complexes." free to MU campus, to others for purchase, 2001. http://wwwlib.umi.com/cr/mo/fullcit?p3036871.

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41

McNeill, Louise. "Functional analysis of the CD8Î² polypeptide and its role in T cell differentiation." Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.324983.

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42

Slessareva, Janna Eugenievna. "Molecular mechanisms of G protein-receptor coupling." Morgantown, W. Va. : [West Virginia University Libraries], 2003. http://etd.wvu.edu/templates/showETD.cfm?recnum=2907.

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Thesis (Ph. D.)--West Virginia University, 2003.
Title from document title page. Document formatted into pages; contains vi, 200 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references.

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43

Ma, Hongzheng. "Molecular mechanisms of G protein-receptor coupling." Morgantown, W. Va. : [West Virginia University Libraries], 2003. http://etd.wvu.edu/templates/showETD.cfm?recnum=2978.

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Thesis (Ph. D.)--West Virginia University, 2003.
Title from document title page. Document formatted into pages; contains viii, 264 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references.

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44

Soper, David Michael. "Interleukin-2 receptor and T cell receptor signaling in regulatory T cells /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/8344.

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45

Doty, Raymond Thomas. "The role of the cytoplasmic tail of antigen-presenting cell surface molecule CD80 in delivery of T cell costimulation /." Thesis, Connect to this title online; UW restricted, 1997. http://hdl.handle.net/1773/8327.

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46

Jobson, Shirley Elizabeth. "DQA1 gene transcription efficiency, its relationship to cell surface DQ antigen expression and disease suscetibility." Thesis, University of Warwick, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.250135.

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47

Standring, Peter. "Class II Human Leukocyte Antigen gene polymorphisms, cell surface expression and immunoglobulin E mediated disease." Thesis, University of Southampton, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.262910.

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48

Josan, Jatinder Singh. "Heteromultivalent Ligands Directed Targeting of Cell-Surface Receptors - Implications in Cancer Diagnostics and Therapeutics." Diss., The University of Arizona, 2008. http://hdl.handle.net/10150/193592.

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Effective detection and treatment of tumor malignancies depends upon identifying targets – molecular markers that differentiate cancer cells from healthy cells. Current cancer therapies involve targeting overexpressed specific gene products. An alternative approach is proposed here: to specifically target combinations of cell-surface receptors using heteromultivalent ligands (htMVLs). There are about 2500 genes encoding for cellsurface proteins in the human genome that can potentially be targeted. Taken as sets, there can be ~ 10⁶ two-receptor combinations and ~ 10⁹ three-receptor combinations available. Our group envisions that using cell-surface protein combinations that are expressed on a cancer cell but not on a normal cell, multivalent constructs displaying complementary ligands of weak affinities can be assembled. These multivalent ligands should bind with high avidity to cancer populations in vivo, and provide a degree of specificity not seen with current approaches. As a proof-of-concept, a series of multivalent ligands were designed and synthesized for a model system consisting of the human Melanocortin subtype 4 receptor (hMC4R) and the Cholecystokinin subtype 2 receptor (CCK-2R). Modeling studies on GPCR dimers predicted that a minimum linker span of 20 - 50 Å would be required to non-covalently crosslink these two receptors. The multivalent ligands were assembled using a modular parallel synthesis approach and using solidphase chemistries. A variety of linkers were explored ranging from highly rigid to highly flexible, and using natural and/or synthetic building blocks. Ligand binding affinities were evaluated using a lanthanide based competitive binding assay in cells that expressed both receptors (bivalent binding) vs those that expressed only one of the receptors (monovalent binding), and were demonstrated to have enhanced binding affinities of up to nearly two orders of magnitude. The promising ligands were further explored by synthesizing fluorescently labeled and/or lanthanide chelate labeled monovalent and heterobivalent ligands designed for in vitro and in vivo studies. More explorative work using these labeled constructs is in progress. To the best of our knowledge, the author believes this is the first such demonstration of a 'synthetic htMVL' directed recruitment and crosslinking of two heterologous cell-surface receptors. This receptor combination approach opens up new possibilities for single cell imaging, cancer detection and therapeutic intervention, and can provide a revolutionary new platform technology with which to direct therapeutics to defined cell populations.

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49

Yeo, Tiong Chia. "Nijmegen breakage syndrome : role of nibrin in antigen receptor gene rearrangement and cellular responses to ionizing radiation /." Thesis, Connect to this title online; UW restricted, 2000. http://hdl.handle.net/1773/8340.

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50

Morrison, Vicky L. "Innate and cognate roles of B cells in T cell differentiation and memory." Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/4873.

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B cells recognise antigens on micro-organisms through their B cell receptor (BCR) and via Toll-like receptors (TLRs), and thus respond in both innate and adaptive manners during the subsequent immune response. Innate recognition through TLRs has the potential to alter the behaviour of whole B cell populations. I show, here, that MyD88-dependent activation of B cells via TLR2 or TLR9 causes the rapid loss of expression of CD62L, by metalloproteinasedependent shedding, resulting in the exclusion of these cells from lymph nodes and Peyer’s patches, but not the spleen. Moreover, systemic infection with Salmonella typhimurium causes shedding of CD62L and the subsequent focussing of B cell migration to the spleen. I reveal that splenic B cells undergo further changes during S. typhimurium infection, including TLR-dependent differentiation of marginal zone B cells into IgM-secreting plasma cells. Together, these TLR-mediated alterations to B cells are likely to influence the development of immunity to pathogens carrying the appropriate ligands. In addition to these innate responses of B cells, endocytosis of cognate antigen through their BCR allows antigen presentation. This, together with their ability to secrete cytokines, means they have the potential to drive T helper cell responses. I investigate the role of B cells in such CD4+ T cell responses by following antigen-specific T cells in vivo, using both a peptide immunisation strategy and the S. typhimurium infection model. I use anti-CD20 B cell depletion antibodies to deplete B cells at various stages of the immune response, and analyse the effects on T follicular helper and memory cell populations. I show that both the generation and maintenance of T follicular helper cells is dependent on the presence of B cells. Furthermore, I demonstrate that B cells are necessary very early in immune responses, during the first 10 days, for efficient generation of memory T cells.

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Dissertations / Theses on the topic 'Cell surface antigen receptors'

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