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J Biol Chem, Vol. 274, Issue 20, 13744-13747, May 14, 1999

COMMUNICATION
Attenuation of Interleukin 2 Signal in the Spleen Cells of Complex Ganglioside-lacking Mice

Jinmin Zhao, Keiko Furukawa^§, Satoshi Fukumoto^§¶, Masahiko Okada, Reiko Furugen^**, Hiroshi Miyazaki^§, Kogo Takamiya, Shinichi Aizawa, Hiroshi Shiku^¶¶, Toshifumi Matsuyama, and Koichi Furukawa^§

From the Departments of  Oncology and  Pediatrics, Nagasaki University School of Medicine and the Departments of ^¶ Pediatric Dentistry and ^** Preventive Dentistry, Nagasaki University School of Dentistry, Sakamoto, Nagasaki, 852-8102, the ^§ Department of Biochemistry II, Nagoya University School of Medicine, Tsurumai, Nagoya, 466-0065,  Laboratory of Morphogenesis, Institute of Molecular Embryology and Genetics, Kumamoto University School of Medicine, Honsho, Kumamoto, 860-0811, and the ^¶¶ Department of Internal Medicine, Mie University School of Medicine, Tsu, Mie, 514-0001 Japan

T cell development and function in complex ganglioside-lacking (GM2/GD2 synthase gene-disrupted) mice were analyzed. GM1, asialo-GM1, and GD1b were representative gangliosides expressed on T cells of the wild type mice and completely deleted on those of the mutant mice. The sizes and cell numbers of the mutant mice spleen and thymus were significantly reduced. Spleen cells from the mutant mice showed clearly reduced proliferation compared with the wild type when stimulated by interleukin 2 (IL-2) but not when treated with concanavalin A or anti-CD3 cross-linking. Expression levels of IL-2 receptor , , and  were almost equivalent, and up-regulation of  chain after T cell activation was also similar between the mutant and wild type mice. Activation of JAK1, JAK3, and SAT5 after IL-2 treatment was reduced, and c-fos expression was delayed and reduced in the mutant spleen cells, suggesting that the IL-2 signal was attenuated in the mutant mice probably due to the modulation of IL-2 receptors by the lack of complex gangliosides.

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