Journal
NATURE MEDICINE
Volume 20, Issue 3, Pages 283-290Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nm.3442
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Funding
- National Health and Medical Research Council of Australia
- Australia Research Council
- Sylvia and Charles Viertel Foundation
- Howard Hughes Medical Institute
- Cancer Council Victoria
- Cancer Australia
- Cancer Council New South Wales
- Leukemia & Lymphoma Society
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Loss of function of the tumor suppressor gene PRDM1 (also known as BLIMP1) or deregulated expression of the oncogene BCL6 occurs in a large proportion of diffuse large B cell lymphoma (DLBCL) cases. However, targeted mutation of either gene in mice leads to only slow and infrequent development of malignant lymphoma, and despite frequent mutation of BCL6 in activated B cells of healthy individuals, lymphoma development is rare. Here we show that T cells prevent the development of overt lymphoma in mice caused by Blimp1 deficiency or overexpression of Bcl6 in the B cell lineage. Impairment of T cell control results in rapid development of DLBCL-like disease, which can be eradicated by polyclonal CD8(+) T cells in a T cell receptor-, CD28- and Fas ligand-dependent manner. Thus, malignant transformation of mature B cells requires mutations that impair intrinsic differentiation processes and permit escape from T cell-mediated tumor surveillance.
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