Skip Navigation


International Immunology Advance Access originally published online on August 16, 2004
International Immunology 2004 16(10):1439-1449; doi:10.1093/intimm/dxh144
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
16/10/1439    most recent
dxh144v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (5)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Takamori, M.
Right arrow Articles by Tokuhisa, T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Takamori, M.
Right arrow Articles by Tokuhisa, T.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?


© 2004 The Japanese Society for Immunology

BAZF is required for activation of naive CD4 T cells by TCR triggering

Mikio Takamori1,2, Masahiko Hatano1, Masafumi Arima1, Akemi Sakamoto1, Lisa Fujimura1, Tety Hartatik1, Takayuki Kuriyama2 and Takeshi Tokuhisa1

1 Department of Developmental Genetics (H2) and 2 Department of Respirology (B2), Graduate School of Medicine, Chiba University, 1-8-1, Inohana, Chuo-ku, Chiba 260-8670, Japan

Correspondence to: T. Tokuhisa; E-mail: tokuhisa{at}faculty.chiba-u.jp

BAZF, a member of the Bcl6 gene family, acts as a sequence-specific transcriptional repressor in association with Bcl6. However, the tissue expression pattern of BAZF differs from that of Bcl6, suggesting a Bcl6-independent function of BAZF. In order to examine the physiological function of BAZF, we generated BAZF-deficient mice and transgenic mice with BAZF-cDNA under the control of the lck proximal promoter (lck-BAZF). These mice were viable and no gross anatomical abnormalities were observed after birth. Since Bcl6 is a key molecule for the generation of memory T cells, we examined the function of T cells of these mice. We show here that cell proliferation of naive CD4 T cells, but not memory ones, of BAZF-deficient mice to anti-CD3 antibody stimulation was impaired. Conversely, cell proliferation of naive CD4 T cells, but not memory ones, of lck-BAZF mice was augmented. Since cell proliferation of naive CD4 T cells of lck-Bcl6 mice to anti-CD3 antibody stimulation was severely impaired, BAZF may attenuate the regulatory effect of Bcl6 on antigenic activation of naive CD4 T cells by Bcl6/BAZF heterodimer formation. These results suggest that BAZF is necessary for activation of naive T cells to antigenic stimulation.

Keywords: cellular activation, knockout, T cell receptor, T lymphocytes, transcription factors, transgenic

Transmitting editor: S. Koyasu


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Mol. Cell. Biol.Home page
H. E. Broxmeyer, S. Sehra, S. Cooper, L. M. Toney, S. Kusam, J. J. Aloor, C. C. Marchal, M. C. Dinauer, and A. L. Dent
Aberrant Regulation of Hematopoiesis by T Cells in BAZF-Deficient Mice
Mol. Cell. Biol., August 1, 2007; 27(15): 5275 - 5285.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
P. M. Manders, P. J. Hunter, A. I. Telaranta, J. M. Carr, J. L. Marshall, M. Carrasco, Y. Murakami, M. J. Palmowski, V. Cerundolo, S. M. Kaech, et al.
Inaugural Article: BCL6b mediates the enhanced magnitude of the secondary response of memory CD8+ T lymphocytes
PNAS, May 24, 2005; 102(21): 7418 - 7425.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.