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A characteristic of the secondary response of CD8(+) T cells that distinguishes it from the primary response is the generation of greater numbers of effector cells. Because effector CD8(+) T cells are derived from a pool of less differentiated, replicating cells in secondary lymphoid organs, and because IL-2 mediates effector differentiation, the enhanced secondary response may reflect the enlargement of this generative pool by the transient repression of IL-2-mediated differentiation. We have examined for this function the transcriptional repressor BCL6b, a homologue of BCL6 that represses IL-2-induced B cell differentiation. BCL6b is expressed in a small subset of antigen-experienced CD8(+) T cells. Ectopic expression of BCL6b in CD8(+) T cells diminishes their growth in response to IL-2 in vitro. Female mice in which the BCL6b gene has been interrupted have normal primary responses of CD8(+) T cells to infection with vaccinia expressing the H-Y epitope, Uty, but Uty-specific, BCL6b(-/-), memory CD8(+) T cells have diminished recall proliferative responses to this epitope in vitro. BCL6b(-/-) mice also have normal primary CD8(+) T cell responses to influenza infection, but nucleoprotein peptide-specific, BCL6b(-/-), memory CD8(+) T cells have a cell autonomous defect in the number of effector cells generated in response to reinfection. Therefore, BCL6b is required for the enhanced magnitude of the secondary response of memory CD8(+) T cells.

Original publication

DOI

10.1073/pnas.0501585102

Type

Journal article

Journal

Proc Natl Acad Sci U S A

Publication Date

24/05/2005

Volume

102

Pages

7418 - 7425

Keywords

Animals, CD8-Positive T-Lymphocytes, Cell Differentiation, DNA Primers, Epitopes, Female, Gene Components, Gene Targeting, Genetic Vectors, H-Y Antigen, Humans, Immunologic Memory, Interferon-gamma, Interleukin-2, Mice, Mice, Knockout, Moloney murine leukemia virus, Repressor Proteins, Reverse Transcriptase Polymerase Chain Reaction, Silencer Elements, Transcriptional, Vaccinia