Fatal leukemia in interleukin-15 transgenic mice

被引:36
|
作者
Fehniger, TA
Suzuki, K
VanDeusen, JB
Cooper, MA
Freud, AG
Caligiuri, MA
机构
[1] Ohio State Univ, Dept Internal Med, Div Hematol Oncol, Columbus, OH 43210 USA
[2] Ohio State Univ, Dept Mol Virol Immunol & Med Genet, Div Human Canc Genet, Columbus, OH 43210 USA
[3] Ohio State Univ, Comphrehens Canc Ctr, Columbus, OH 43210 USA
[4] Gunma Univ, Sch Med, Dept Urol, Gunma, Japan
关键词
D O I
10.1006/bcmd.2001.0379
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The role of inflammation in the early genesis of certain malignancies has recently been appreciated. Interleukin (IL)-15, a proinflammatory cytokine and growth factor, is required for lymphocyte homeostasis. Intriguingly, the expression of IL-15 protein is tightly controlled by multiple posttranscriptional mechanisms, suggesting that inappropriate expression of IL-15 may be detrimental to the host. We recently engineered a transgenic mouse in which the normal posttranscriptional control of IL-15 is eliminated, thereby overexpressing the murine IL-15 protein. IL-15 transgenic mice have early expansions in NK and CD8(+) T lymphocytes and later develop fatal lymphocytic leukemia with a T-NK phenotype. This article recapitulates the phenotype of these IL-15 transgenic mice and discusses the utility of this model as a tool to further our understanding of leukemogenesis. (C) 2001 Academic Press.
引用
收藏
页码:223 / 230
页数:8
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