期刊
IMMUNOLOGY AND CELL BIOLOGY
卷 100, 期 9, 页码 705-717出版社
WILEY
DOI: 10.1111/imcb.12578
关键词
B cell malignancy; BCL6; CD137L; CD4 T cells; tumor immunity
资金
- National Health and Medical Research Council (NHMRC) Australia Investigator Award [APP1175411]
- NHMRC Project Grant [1085156]
- Swedish Research Council [2016-06659]
- Early Postdoc Mobility fellowship [P2ZHP3_164964]
- Advanced Postdoc Mobility fellowship [P300PA_177893]
- Swiss National Science Foundation
- Peter Doherty Early Career fellowship [APP1145136]
- NHMRC Australia
- NHMRC [APP1185294]
- Monash Bridging Postdoctoral Fellowship
- Swiss National Science Foundation (SNF) [P2ZHP3_164964, P300PA_177893] Funding Source: Swiss National Science Foundation (SNF)
- Swedish Research Council [2016-06659] Funding Source: Swedish Research Council
Aberrant expression of BCL6 drives tumorigenesis in DLBCL. CD4 T cells contribute to immune surveillance and control lymphoproliferative disease in lymphoma-prone mice, with CD137L signaling playing a key role.
Aberrant expression of the proto-oncogene BCL6 is a driver of tumorigenesis in diffuse large B cell lymphoma (DLBCL). Mice overexpressing BCL6 from the B cell-specific immunoglobulin heavy chain mu intron promoter (I mu-Bcl6(Tg/+)) develop B cell lymphomas with features typical of human DLBCL. While the development of B cell lymphoma in these mice is tightly controlled by T cells, the mechanisms of this immune surveillance are poorly understood. Here we show that CD4 T cells contribute to the control of lymphoproliferative disease in lymphoma-prone I mu-Bcl6(Tg/+) mice. We reveal that this CD4 T cell immuno-surveillance requires signaling by the co-stimulatory molecule CD137 ligand (CD137L; also known as 4-1BBL), which may promote the transition of pre-malignant B cells with an activated phenotype into the germinal center stage via reverse signaling, preventing their hazardous accumulation. Thus, CD137L-mediated CD4 T cell immuno-surveillance adds another layer of protection against B cell malignancy to that provided by CD8 T cell cytotoxicity.
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