Fatal leukemia in interleukin-15 transgenic mice.
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.
Fehniger
T A
TA
Department of Internal Medicine, Ohio State University, Columbus, Ohio 43210, USA.
Suzuki
K
K
VanDeusen
J B
JB
Cooper
M A
MA
Freud
A G
AG
Caligiuri
M A
MA
D000818:Animals; D002471:Cell Transformation, Neoplastic / Q000187:drug effects; D004195:Disease Models, Animal; D006801:Humans; D019409:Interleukin-15 / Q000009:adverse effects* / Q000235:genetics; D007694:Killer Cells, Natural; D015458:Leukemia, T-Cell / Q000209:etiology* / Q000401:mortality; D051379:Mice; D008822:Mice, Transgenic
D019409:Interleukin-15