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International Immunology, Vol. 11, No. 7, 1035-1042, July 1999
© 1999 Japanese Society for Immunology

Severe impairment of B cell function in lpr/lpr mice expressing transgenic Fas selectively on B cells

Hajime Komano1, Yuko Ikegami1, Minesuke Yokoyama2, Rika Suzuki2, Shin Yonehara3, Yoshiki Yamasaki4 and Nobukata Shinohara1,5

1 Department of Immunology and
2 Reproductive Engineering Section, Mitsubishi Kasei Institute of Life Sciences, Machida, Japan
3 Institute for Virus Research, Kyoto University, Kyoto, Japan
4 The Pharmaceutical Basic Research Laboratories, JT Inc., Yokohama, Japan
5 Department of Immunology, Kitasato University School of Medicine, Sagamihara, Kanagawa 228, Japan

Correspondence to: N. Shinohara, Department of Immunology, Kitasato University School of Medicine, 1-15-1 Kitasato, Sagamihara, Kanagawa 228-8555, Japan

Transgenic lpr/lpr mice expressing functional Fas selectively on B cells were produced in an attempt to elucidate the role of Fas on B cells in the regulation of autoantibody production. The homozygous lpr/lpr mice carrying the transgene did not produce anti-double-stranded DNA antibodies throughout their lives, whereas the development of abnormal lpr T cells (double negative, B220+) was not suppressed. Further analyses, however, revealed that the expression of the transgenic Fas on B cells of lpr/lpr homozygous mice resulted in severe impairment of the B cell function. The defect was characterized by a decrease in the number of mature peripheral B cells, a reduction in the serum Ig level and the total failure of B cells to mount antibody responses to stimulations of T-dependent as well as T-independent antigens. Such a defect was prominent only when the transgene was expressed on the lpr/lpr homozygous background. On the contrary, B cells of the transgenic lpr/lpr mice were shown to be capable of producing Ig when stimulated with anti-CD40 in the presence of IL-4 and IL-5. Furthermore, lpr/lpr T cells showed enhanced non-specific cytolytic activity. These observations suggested that the observed B cell defect was probably attributable to the destruction of activated B cells expressing transgenic Fas by aggressive lpr/lpr T cells.

Keywords: autoantibody, B cell, Fas, lpr

Transmitting editor: K. Okumura


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