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International Immunology Advance Access originally published online on February 16, 2007
International Immunology 2007 19(4):427-433; doi:10.1093/intimm/dxm007
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© 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.


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