The role of inflammation in the early genesis of certain malignancies has r
ecently been appreciated. Interleukin (IL)-15, a proinflammatory cytokine a
nd growth factor, is required for lymphocyte homeostasis. Intriguingly, the
expression of IL-15 protein is tightly controlled by multiple posttranscri
ptional mechanisms, suggesting that inappropriate expression of IL-15 may b
e detrimental to the host. We recently engineered a transgenic mouse in whi
ch the normal posttranscriptional control of IL-15 is eliminated, thereby o
verexpressing the murine IL-15 protein. IL-15 transgenic mice have early ex
pansions in NK and CD8(+) T lymphocytes and later develop fatal lymphocytic
leukemia with a T-NK phenotype. This article recapitulates the phenotype o
f these IL-15 transgenic mice and discusses the utility of this model as a
tool to further our understanding of leukemogenesis. (C) 2001 Academic Pres
s.