{"id":{"repo_id":"birmingham","oai_identifier":"oai:etheses.bham.ac.uk:930"},"canonical_url":"https://search.dev.ndltd.org/etd/birmingham/oai:etheses.bham.ac.uk:930","repository":{"repo_id":"birmingham","name":"University of Birmingham","base_url":"https://etheses.bham.ac.uk/cgi/oai2"},"display":{"title":"The exploitation of neuronal survival factors in Burkitt’s lymphoma and germinal centre B cells","abstract":"Neurotrophins are neuromodulatory proteins utilised within neuronal networks for development and survival. Based on previous evidence revealing the expression of neurotrophin components in immune cells, the present study investigates neurotrophin component expression within Burkitt’s Lymphoma B cells. Different latency stages within Burkitt’s Lymphoma B cells are observed due to the expression of resident EBV latency genes. These B cells are said to display germinal centre B cell markers and interact with other cells within a germinal centre environment, such as Follicular Dendritic Cells (FDCs) and T cells. EBV latency phenotypes were characterised for the lines used here; these lines were then screened for the expression of neurotrophin ligands and their receptors: the selective high affinity Tropomyosin receptor kinases TrkA, TrkB and TrkC and the (common) low affinity, tumour necrosis factor receptor member, p75NTR. FDC-like cell lines were also analysed for neurotrophin component expression. This was to question FDCs as potential providers of paracrine neurotrophin signalling to Burkitt’s lymphoma B cells. Neurotrophin and neurotrophin receptor expression was detected by flow cytometry, confocal microscopy, reverse transcription polymerase chain reaction (PCR) and real time PCR methods. Cell lines with the full complement of EBV latency genes expressed were positive for the neurotrophin, Brain Derived Neurotrophic Factor (BDNF) and all neurotrophin receptors in question. Burkitt’s lymphoma cells expressing limited EBV latency genes revealed more restricted expression of neurotrophin components. FDC-like lines also express neurotrophin and neurotrophin receptors, thus paracrine signalling between Burkitt’s lymphoma cells and FDCs may occur via this axis, perhaps to enhance B cell survival.","abstract_html":"Neurotrophins are neuromodulatory proteins utilised within neuronal networks for development and survival. Based on previous evidence revealing the expression of neurotrophin components in immune cells, the present study investigates neurotrophin component expression within Burkitt’s Lymphoma B cells. Different latency stages within Burkitt’s Lymphoma B cells are observed due to the expression of resident EBV latency genes. These B cells are said to display germinal centre B cell markers and interact with other cells within a germinal centre environment, such as Follicular Dendritic Cells (FDCs) and T cells. EBV latency phenotypes were characterised for the lines used here; these lines were then screened for the expression of neurotrophin ligands and their receptors: the selective high affinity Tropomyosin receptor kinases TrkA, TrkB and TrkC and the (common) low affinity, tumour necrosis factor receptor member, p75NTR. FDC-like cell lines were also analysed for neurotrophin component expression. This was to question FDCs as potential providers of paracrine neurotrophin signalling to Burkitt’s lymphoma B cells. Neurotrophin and neurotrophin receptor expression was detected by flow cytometry, confocal microscopy, reverse transcription polymerase chain reaction (PCR) and real time PCR methods. Cell lines with the full complement of EBV latency genes expressed were positive for the neurotrophin, Brain Derived Neurotrophic Factor (BDNF) and all neurotrophin receptors in question. Burkitt’s lymphoma cells expressing limited EBV latency genes revealed more restricted expression of neurotrophin components. FDC-like lines also express neurotrophin and neurotrophin receptors, thus paracrine signalling between Burkitt’s lymphoma cells and FDCs may occur via this axis, perhaps to enhance B cell survival.","abstract_has_math":false,"creators":["Chirimuuta, Fungai Natalie Winnie"],"institution":"University of Birmingham","degree_name":"d_ph","degree_level":"d_ph","degree_discipline":null,"degree_department":null,"school":null,"contributors":[],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2010,"date_issued":"2010-07","date_published":"2010-07","updated_at":"2026-07-24T01:11:15Z","subjects":["R Medicine (General)"],"languages":[],"rights":[],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":null,"outbound_label":null,"outbound_source":null},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor.sponsor","label":"Sponsor","values":["na"]},{"key":"dc:creator","label":"Author","values":["Chirimuuta, Fungai Natalie Winnie"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2010-07"]},{"key":"dc:date.issued","label":"Date","values":["2010-07"]},{"key":"dc:publisher.department","label":"Dc Publisher Department","values":["College of Medical & Dental Sciences","School of Immunity and Infection"]},{"key":"dc:publisher.institution","label":"Dc Publisher Institution","values":["University of Birmingham"]},{"key":"dc:relation.isreferencedby","label":"Dc Relation Isreferencedby","values":["http://etheses.bham.ac.uk//id/eprint/930/"]},{"key":"dc:type","label":"Dc Type","values":["Thesis"]},{"key":"dc:type.qualificationlevel","label":"Dc Type Qualificationlevel","values":["d_ph"]},{"key":"dc:type.qualificationname","label":"Dc Type Qualificationname","values":["d_ph"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["R Medicine (General)"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier.uri","label":"Identifier URI","values":["http://etheses.bham.ac.uk//id/eprint/930/2/Chirimuuta_10_PhD.pdf","http://etheses.bham.ac.uk//id/eprint/930/1/Decl_IS_Chirimuta_10PhD.pdf"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["Neurotrophins are neuromodulatory proteins utilised within neuronal networks for development and survival. Based on previous evidence revealing the expression of neurotrophin components in immune cells, the present study investigates neurotrophin component expression within Burkitt’s Lymphoma B cells. Different latency stages within Burkitt’s Lymphoma B cells are observed due to the expression of resident EBV latency genes. These B cells are said to display germinal centre B cell markers and interact with other cells within a germinal centre environment, such as Follicular Dendritic Cells (FDCs) and T cells. EBV latency phenotypes were characterised for the lines used here; these lines were then screened for the expression of neurotrophin ligands and their receptors: the selective high affinity Tropomyosin receptor kinases TrkA, TrkB and TrkC and the (common) low affinity, tumour necrosis factor receptor member, p75NTR. FDC-like cell lines were also analysed for neurotrophin component expression. This was to question FDCs as potential providers of paracrine neurotrophin signalling to Burkitt’s lymphoma B cells. Neurotrophin and neurotrophin receptor expression was detected by flow cytometry, confocal microscopy, reverse transcription polymerase chain reaction (PCR) and real time PCR methods. Cell lines with the full complement of EBV latency genes expressed were positive for the neurotrophin, Brain Derived Neurotrophic Factor (BDNF) and all neurotrophin receptors in question. Burkitt’s lymphoma cells expressing limited EBV latency genes revealed more restricted expression of neurotrophin components. FDC-like lines also express neurotrophin and neurotrophin receptors, thus paracrine signalling between Burkitt’s lymphoma cells and FDCs may occur via this axis, perhaps to enhance B cell survival."]},{"key":"dc:format","label":"Dc Format","values":["application/pdf"]},{"key":"dc:title","label":"Title","values":["The exploitation of neuronal survival factors in Burkitt’s lymphoma and germinal centre B cells"]}]}],"canonical_facts":{"dc:contributor.sponsor":["na"],"dc:creator":["Chirimuuta, Fungai Natalie Winnie"],"dc:date":["2010-07"],"dc:date.issued":["2010-07"],"dc:description.abstract":["Neurotrophins are neuromodulatory proteins utilised within neuronal networks for development and survival. Based on previous evidence revealing the expression of neurotrophin components in immune cells, the present study investigates neurotrophin component expression within Burkitt’s Lymphoma B cells. Different latency stages within Burkitt’s Lymphoma B cells are observed due to the expression of resident EBV latency genes. These B cells are said to display germinal centre B cell markers and interact with other cells within a germinal centre environment, such as Follicular Dendritic Cells (FDCs) and T cells. EBV latency phenotypes were characterised for the lines used here; these lines were then screened for the expression of neurotrophin ligands and their receptors: the selective high affinity Tropomyosin receptor kinases TrkA, TrkB and TrkC and the (common) low affinity, tumour necrosis factor receptor member, p75NTR. FDC-like cell lines were also analysed for neurotrophin component expression. This was to question FDCs as potential providers of paracrine neurotrophin signalling to Burkitt’s lymphoma B cells. Neurotrophin and neurotrophin receptor expression was detected by flow cytometry, confocal microscopy, reverse transcription polymerase chain reaction (PCR) and real time PCR methods. Cell lines with the full complement of EBV latency genes expressed were positive for the neurotrophin, Brain Derived Neurotrophic Factor (BDNF) and all neurotrophin receptors in question. Burkitt’s lymphoma cells expressing limited EBV latency genes revealed more restricted expression of neurotrophin components. FDC-like lines also express neurotrophin and neurotrophin receptors, thus paracrine signalling between Burkitt’s lymphoma cells and FDCs may occur via this axis, perhaps to enhance B cell survival."],"dc:format":["application/pdf"],"dc:identifier.uri":["http://etheses.bham.ac.uk//id/eprint/930/2/Chirimuuta_10_PhD.pdf","http://etheses.bham.ac.uk//id/eprint/930/1/Decl_IS_Chirimuta_10PhD.pdf"],"dc:publisher.department":["College of Medical & Dental Sciences","School of Immunity and Infection"],"dc:publisher.institution":["University of Birmingham"],"dc:relation.isreferencedby":["http://etheses.bham.ac.uk//id/eprint/930/"],"dc:subject":["R Medicine (General)"],"dc:title":["The exploitation of neuronal survival factors in Burkitt’s lymphoma and germinal centre B cells"],"dc:type":["Thesis"],"dc:type.qualificationlevel":["d_ph"],"dc:type.qualificationname":["d_ph"]},"updated_at":"2026-07-24T01:11:15Z"}