The Journal of Experimental Medicine
VeriKine-HS Human IFN-Beta
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J. Exp. Med.
© The Rockefeller University Press
0022-1007/97/02/791/04 $2.00
Volume 185, Number 4, February 17, 1997 791-794

BRIEF DEFINITIVE REPORT:
Effects of Breeding Environments on Generation and Activation of Autoreactive B-1 Cells in Anti-red Blood Cell Autoantibody Transgenic Mice

By Masao Murakami,* Kazuo Nakajima,Dagger Ken-ichi Yamazaki,Dagger Takehiko Muraguchi,Dagger Tadao Serikawa,Dagger and Tasuku Honjo*

From the * Department of Medical Chemistry, Kyoto University Faculty of Medicine, Sakyo-ku Yoshida, Kyoto 606, Japan; Dagger  Institute of Laboratory Animals, Kyoto University Faculty of Medicine, Sakyo-ku Yoshida, Kyoto 606, Japan

In anti-red blood cell autoantibody transgenic (autoAb Tg) mice almost all B cells are deleted except for B-1 cells in the peritoneal cavity and the gut. About one-half of the auto Ab Tg mice suffer from autoimmune hemolytic anemia (AIHA) in the conventional condition. Oral administration of lipopolysaccharides activates B-1 cells and induces autoimmune symptoms in the Tg mice, suggesting that the autoimmune disease in anti-RBC autoAb Tg mice is triggered by infections. To examine the association of bacterial infections with the generation of B-1 cells and the occurrence of the autoimmune disease, we analyzed anti-RBC autoAb Tg mice bred in germ-free and specific pathogen-free conditions. In germ-free conditions, few peritoneal B-1 cells were detected, while a significant number of peritoneal B-1 cells existed in specific pathogen-free conditions. In both conditions, no mice suffered from AIHA. However, when these Tg mice were transferred to the conventional condition or injected with lipopolysaccharide, peritoneal B-1 cells expanded and some of these mice suffered from AIHA. These results clearly showed that bacterial infections are responsible for both the expansion of B-1 cells and the onset of the autoimmune disease in these Tg mice.


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