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This dissertation, Dendritic Cell Biology Regulated by Epstein-Barr Virus (EBV) and Its Associated Tumors by Ting, Chen, 陳楟, was obtained from The University of Hong Kong (Pokfulam, Hong Kong) and is being sold pursuant to Creative Commons: Attribution 3.0 Hong Kong License. The content of this dissertation has not been altered in any way. We have altered the formatting in order to facilitate the ease of printing and reading of the dissertation. All rights not granted by the above license are retained by the author. Abstract: Abstract of thesis entitled Dendritic cell biology regulated by Epstein-Barr virus (EBV) and its associated tumors Submitted by Ting Chen for the degree of Master of Philosophy at The University of Hong Kong in August 2004 Dendritic cells (DCs) are professional antigen-presenting cells that possess unique ability to regulate both innate and adaptive immunity. They patrol in peripheral tissues, uptake, process and present self and non-self antigens. DCs also regulate T and B lymphocytes immunity. Furthermore, DC-based immunotherapy has been investigated from laboratory to clinical trials. Functions of DCs are characterized and correlated with their surface phenotypic markers and chemokine receptors. Expression of chemokine receptors is closely involved in DCs migration, and the capacity of DCs to initiate immune responses is highly dependent on their migratory properties. These surface molecules expression varies at different stages of differentiation and are closely related with DCs immunological functions and induction of the antigen-specific immunity. Epstein-Barr virus (EBV) is one of the eight known gamma herpesviruses. It infects more than 90% of the human adult population with lifelong infection. The infection usually occurs in early childhood. Moreover, EBV is the first human virus to be directly implicated in carcinogenesis, for example, nasopharyngeal carcinoma (NPC), Burkitt's lymphoma (BL) and Hodgkin's disease (HD) etc. EBV has two major target cells in vivo: B lymphocytes and epithelium cells. EBV has the ability to convert normal resting B lymphocytes into permanently growing lymphoblastoid cells. Because of its great impact on human health, it has been of great interest to understand how EBV and its associated tumors escape immune surveillance. In order to delineate DC pathophysiology in EBV infection, the expression of six phenotypic markers (CD83, CD86, CD40, HLA-DR, CD11c and CD14) and two chemokine receptors (CCR5 and CXCR4) were assessed after exposure of DCs at different stages of differentiation (monocytes, differentiating DCs and differentiated DCs) to in vitro propagated EBV culture or EBV-associated tumors supernatant environment. Dendritic cells exposed to in vitro propagated EBV culture supernatant or EBV-associated tumors supernatant shown alternative phenotypic features at different differentiation phases. For example, EBV-cultured cell supernatant mainly activated the phenotype of differentiating DCs, i.e., monocyte-derived DCs cultured to D4 to D5, while the secretory factors in the EBV-associated tumor culture supernatant activated differentiated DCs (cultured D7 to D8). These activating effects, by contrast, were not noticeable on monocytes. These findings showed, for the first time, that DCs phenotypic characteristics are modulated by EBV and its in vitro culture supernatant, as well as by the EBV-associated tumors. Furthermore, DCs co-cultured with EBV harboring cells (B95.8) or EBV-associated tumor cells underwent excessive apoptosis after overnight co-culture, compared with co-culture with EBV (-) B cell tumors. This may indicate an alternative pathway that EBV and its associated tumors may employ to escape from DCs surveillance through induction of premature and excessive DC death. It is therefore likely that the reduction of DC numbers after cell-cell contact with these EBV (+) tumors affect EBV-specific immunity accordin

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