Immunological characterization of C3H mice congenic for Faslprcg, C3H/HeJ-Faslprcg/Faslprcg

被引:6
作者
Yasuda, T
Zhang, Y
Nagase, H
Kaneko, T
Sayama, K
Hashimoto, H
Matsuzawa, A [1 ]
机构
[1] Univ Tokyo, Inst Med Sci, Lab Anim Res Ctr, Minato Ku, Tokyo 1068639, Japan
[2] Shinshu Univ, Sch Med, Dept Parasitol, Matsumoto, Nagano 3908621, Japan
[3] Shizuoka Univ, Fac Agr, Dept Anim Sci, Ohya, Shizuoka 4228529, Japan
[4] Mijigakuin Univ, Lab Gen Biol, Totsuka Ku, Yokohama, Kanagawa 2440816, Japan
关键词
Fas(lprcg); Fas mutations; autoimmunity; lymphadenopathy; C3H background;
D O I
10.1258/002367700780578019
中图分类号
S85 [动物医学(兽医学)];
学科分类号
0906 ;
摘要
Fas(Ipr) (1pr) and Fas(1prcg) (1pr(cg)) are allelic mutations of the Fas gene that is involved in apoptosis or programmed cell death. 1pr greatly reduces the expression of functional Fas and 1pr(cg) expresses the death domain-disabled, non-functional Fas on the cell surface. C3H/HeJ mice congenic for 1prcg (C3H-1pr(cg)) were established and compared with C3H/HeJ-1pr/1pr (C3H-1pr) mice for their immunological and pathological features. Lymphadenopathy, splenomegaly, development of CD4(-)CD8(-)B220(+) or double-negative (DN) T cells, renal pathology, and lymphoid cell infiltration in the lung and liver were not significantly different between C3H-1pr(cg) and C3H-1pr mice. Noticeably, however, the production of serum immunoglobulin, autoantibodies against double-strand DNA and serum immune complexes were significantly lower in C3H-1pr(cg) than in C3H-1pr mice. The results indicate that the death signal through the death domain of Fas is responsible for lymphoproliferation due to the accumulation of DN T cells and suggest that the region of Fas outside the death domain may be involved in autoantibody production. The newly-developed congenic C3H-1pr(cg) mice will provide a powerful tool for research into the function of Fas apart from apoptosis.
引用
收藏
页码:46 / 55
页数:10
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