BCL6b mediates the enhanced magnitude of the secondary response of memory CD8+ T lymphocytes

Autor: Marlene J. Carrasco, Aino I. Telaranta, James M. Carr, Susan M. Kaech, Douglas T. Fearon, Vincenzo Cerundolo, Peter M. Manders, Patricia J. Hunter, Jennifer L. Marshall, Yusuke Murakami, Rafi Ahmed, Michael J. Palmowski
Jazyk: angličtina
Rok vydání: 2005
Předmět:
Zdroj: Proceedings of the National Academy of Sciences of the United States of America. 102(21)
ISSN: 1091-6490
0027-8424
Popis: 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.
Databáze: OpenAIRE