Fatal leukemia in interleukin-15 transgenic mice

Todd A. Fehniger, Kazuhiro Suzuki, Jeffrey B. VanDeusen, Megan A. Cooper, Aharon G. Freud, Michael A. Caligiuri

Research output: Contribution to journalArticle

36 Scopus citations

Abstract

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.

Original languageEnglish
Pages (from-to)223-230
Number of pages8
JournalBlood Cells, Molecules, and Diseases
Volume27
Issue number1
DOIs
StatePublished - Jan 1 2001
Externally publishedYes

Fingerprint Dive into the research topics of 'Fatal leukemia in interleukin-15 transgenic mice'. Together they form a unique fingerprint.

  • Cite this