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Leukemia/lymphoma development in IL-15-deficient TCR-transgenic mice

Sporadic mouse tumor models are valuable tools to understand disease development and treatment efficacies. Here we show that a transgenic T cell receptor expression predisposes mice to leukemia/lymphoma development. Leukemia/lymphoma precursors expressed low amounts of MHC class I and were deleted by NK cells in immunocompetent mice resulting in increased tumor frequency under NK cell absence. Leukemias/lymphomas were clonal and regrow after transfers into NK cell-deficient hosts. Phenotypically, most leukemias/lymphomas were positive for CD3 and CD8, and all expressed high levels of the co-stimulatory molecules PD1, ICOS and CD28 as well as of CD30 resembling the phenotype of immature CD8 single-positive thymocytes. Half of the leukemias/lymphomas harbored Notch1 mutations. Dendritic cells appear to have an auxiliary role in leukemia/lymphomagenesis since their deletion caused decreased tumor growth. The study of leukemias/lymphomas in IL-15-deficient TCR-transgenic mice may help to further understand T cell lymphomagenesis, the role of lymphoma environment, and may be useful to design and test treatments.

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Correspondence to Sigrid Dubois.

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This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Keywords

  • Mouse Tumor
  • Test Treatment
  • Mouse Tumor Model
  • Immunocompetent Mouse
  • Tumor Frequency