Skip Navigation


International Immunology Advance Access originally published online on February 16, 2007
International Immunology 2007 19(4):427-433; doi:10.1093/intimm/dxm007
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
19/4/427    most recent
dxm007v1
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 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 (2)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Ichii, H.
Right arrow Articles by Tokuhisa, T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ichii, H.
Right arrow Articles by Tokuhisa, T.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?


© The Japanese Society for Immunology. 2007. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Bcl6 is essential for the generation of long-term memory CD4+ T cells

Hirohito Ichii1,2,3,5, Akemi Sakamoto1, Masafumi Arima1, Masahiko Hatano1,4, Yoshikazu Kuroda2 and Takeshi Tokuhisa1

1 Department of Developmental Genetics (H2), Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan
2 Department of Gastroenterological Surgery, Kobe University Graduate School of Medical Sciences, Kobe 650-0017, Japan
3 Japan Society for the Promotion of Science, 8 Ichiban-chou, Chiyoda-Ku, Tokyo 102-8472, Japan
4 Biomedical Research Center, Chiba University, Chiba 260-8670, Japan
5 Present address: Diabetes Research Institute, University of Miami, Leonard Miller School of Medicine, 1450 Northwest 10th Avenue, Miami, FL 33136, USA

Correspondence to: A. Sakamoto; E-mail: sakamoto{at}faculty.chiba-u.jp

Bcl6 plays a role in the generation and maintenance of memory CD8+ T cells. We analyzed here a role for Bcl6 in the generation of long-term memory CD4+ T cells. Naive CD45RB+ CD4+ T cells from Bcl6-deficient DO11.10 (KJ1.26+) transgenic mice were transferred into BALB/c mice and immunized with ovalbumin peptide and LPS. Long-term memory KJ1.26+ CD4+ T cells from wild-type mice were detected in the spleen, lungs and liver during 10 weeks after immunization; however, Bcl6-deficient KJ1.26+ CD4+ T cells were vanished completely in those organs 4 weeks after immunization. Since memory CD4+ T cells can be generated from effector CD4+ T cells, properties of Bcl6-deficient effector CD4+ T cells were compared with those wild-type effector CD4+ T cells 10 days after immunization. Numbers of IFN-{gamma}-non-producing CD45RB–, CD62L+ or IL-7R{alpha}+ effector CD4+ T cells in the spleen, lungs and liver were similar between Bcl6-deficient and wild-type CD4+ T cells. However, the percentage of apoptotic cells in Bcl6-deficient effector CD4+ T cells was higher than that in wild-type effector CD4+ T cells. At the late effector phase, the number of IFN-{gamma}-non-producing cells and the percentage of apoptotic cells in Bcl6-deficient CD4+ T cells were smaller and higher than those in wild-type CD4+ T cells, respectively. These data suggest that Bcl6 in CD4+ T cells plays a role in protection of memory precursor CD4+ T cells from apoptosis and may involve in survivability of long-term memory CD4+ T cells.

Keywords: CD4+ T lymphocyte, TCR transgenic, Th, transcription factors

Transmitting editor: T. Watanabe

Received 26 May 2006, accepted 16 January 2007.


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




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.