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Title: A role for BCL6b transcription factor in CD8+ T cell secondary expansion and memory
Author: Hunter, Patricia Jean
Awarding Body: University of Cambridge
Current Institution: University of Cambridge
Date of Award: 2004
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Lymphocyte development following encounter with microbial antigen is driven by the need to combat infection over the short and long term. This requires the generation and expansion of cells capable of immediate effector function as well as a population that endures to combat chronic infection or the reappearance of the same infection at a later time. BCL6b is a POZ family transcription factor and close homologue of BCL6. We found increased expression of BCL6b in memory compared to naïve CD8+ T cells. BCL6b deficient mice were generated by gene targeting in order to determine its function. In comparing wild type and BCL6b deficient CD8+ T cells, we demonstrated equivalent cytotoxicity and IFN-g production in individual antigen-specific cells. However, following a second challenge with antigen, BCL6b deficient CD8+ T cells failed to undergo proliferative expansion and significantly fewer antigen-specific cells were present at the end of the response compared with wild type. Therefore, BCL6b is required for the development of CD8+ T cells capable of expanding in response to secondary immune stimulation. By analogy to BCL6, which suppresses terminal differentiation in B cells, BCL6b may create a self-renewing stage of CD8+ T cell development that enables the continuous generation of effector T cells to combat sporadic or chronic infection over the lifetime of the host.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID:  DOI: Not available