NDLI: Oncogenic Transformation of Dendritic Cells and Their Precursors Leads to Rapid Cancer Development in Mice.

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Oncogenic Transformation of Dendritic Cells and Their Precursors Leads to Rapid Cancer Development in Mice.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Böttcher, Jan P. Helft, Julie Zelenay, Santiago Rogers, Neil C. Schraml, Barbara U. Reis e Sousa, Caetano
Description	Country affiliation: United kingdom Author Affiliation: Böttcher JP ( Immunobiology Laboratory, The Francis Crick Institute, Lincoln's Inn Fields Laboratory, London WC2A 3LY, United Kingdom.); Zelenay S ( Immunobiology Laboratory, The Francis Crick Institute, Lincoln's Inn Fields Laboratory, London WC2A 3LY, United Kingdom.); Rogers NC ( Immunobiology Laboratory, The Francis Crick Institute, Lincoln's Inn Fields Laboratory, London WC2A 3LY, United Kingdom.); Helft J ( Immunobiology Laboratory, The Francis Crick Institute, Lincoln's Inn Fields Laboratory, London WC2A 3LY, United Kingdom.); Schraml BU ( Immunobiology Laboratory, The Francis Crick Institute, Lincoln's Inn Fields Laboratory, London WC2A 3LY, United Kingdom.); Reis e Sousa C ( Immunobiology Laboratory, The Francis Crick Institute, Lincoln's Inn Fields Laboratory, London WC2A 3LY, United Kingdom caetano@crick.ac.uk.)
Abstract	Dendritic cells (DCs) are powerful APCs that can induce Ag-specific adaptive immune responses and are increasingly recognized as important players in innate immunity to both infection and malignancy. Interestingly, although there are multiple described hematological malignancies, DC cancers are rarely observed in humans. Whether this is linked to the immunogenic potential of DCs, which might render them uniquely susceptible to immune control upon neoplastic transformation, has not been fully investigated. To address the issue, we generated a genetically engineered mouse model in which expression of Cre recombinase driven by the C-type lectin domain family 9, member a (Clec9a) locus causes expression of the Kirsten rat sarcoma viral oncogene homolog (Kras)(G12D) oncogenic driver and deletion of the tumor suppressor p53 within developing and differentiated DCs. We show that these Clec9a(Kras-G12D) mice rapidly succumb from disease and display massive accumulation of transformed DCs in multiple organs. In bone marrow chimeras, the development of DC cancer could be induced by a small number of transformed cells and was not prevented by the presence of untransformed DCs. Notably, activation of transformed DCs did not happen spontaneously but could be induced upon stimulation. Although Clec9a(Kras-G12D) mice showed altered thymic T cell development, peripheral T cells were largely unaffected during DC cancer development. Interestingly, transformed DCs were rejected upon adoptive transfer into wild-type but not lymphocyte-deficient mice, indicating that immunological control of DC cancer is in principle possible but does not occur during spontaneous generation in Clec9a(Kras-G12D) mice. Our findings suggest that neoplastic transformation of DCs does not by default induce anti-cancer immunity and can develop unhindered by immunological barriers.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1500889
Journal	The Journal of Immunology
Issue Number	10
Volume Number	195
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2015-11-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Cell Transformation, Neoplastic Immunology Dendritic Cells Neoplasms, Experimental Stem Cells Animals Genetics Pathology Lectins, C-type Mice Mice, Transgenic Proto-oncogene Proteins P21(ras) Receptors, Immunologic Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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