The Journal of Experimental Medicine
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J. Exp. Med.
© The Rockefeller University Press
0022-1007/97/08/439/10 $2.00
Volume 186, Number 3, August 4, 1997 439-448

Disruption of the Bcl6 Gene Results in an Impaired Germinal Center Formation

By Tetsuya Fukuda,*Dagger Takehiko Yoshida,* Seiji Okada,* Masahiko Hatano,* Tohru Miki,Dagger Kazuki Ishibashi,* Shinichiro Okabe,* Haruhiko Koseki,§ Shinsaku Hirosawa,Dagger Masaru Taniguchi,§ Nobuyuki Miyasaka,Dagger and Takeshi Tokuhisa*

From the * Division of Developmental Genetics, Center for Biomedical Science, Chiba University School of Medicine, Chiba 260, Japan; the Dagger  First Department of Internal Medicine, Tokyo Medical and Dental University, Tokyo 113, Japan; and the § Core Research for Evolutional Science and Technology, Division of Molecular Immunology, Center for Biomedical Science, Chiba University School of Medicine, Chiba 260, Japan

The Bcl6 gene has been identified from the chromosomal translocation breakpoint in B cell lymphomas, and its products are expressed highly in germinal center (GC) B cells. To investigate the function of Bcl6 in lymphocytes, we have generated RAG1-deficient mice reconstituted with bone marrow cells from Bcl6-deficient mice (Bcl6-/-RM). Lymphogenesis in primary lymphoid tissues of Bcl6-/-RM is normal, and Bcl6-/-RM produced control levels of primary IgG1 antibodies specific to T cell-dependent antigens. However, GCs were not found in these mice. This defect was mainly due to the abnormalities of B cells. Therefore, Bcl6 is essential for the differentiation of GC B cells.


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