Journal article
Interleukin-12 from CD103 Batf3-dependent dendritic cells required for NK-cell suppression of metastasis
D Mittal, D Vijayan, EM Putz, AR Aguilera, KA Markey, J Straube, S Kazakoff, SL Nutt, K Takeda, GR Hill, N Waddell, MJ Smyth
Cancer Immunology Research | AMER ASSOC CANCER RESEARCH | Published : 2017
Abstract
Several host factors may affect the spread of cancer to distant organs; however, the intrinsic role of dendritic cells (DC) in controlling metastasis is poorly described. Here, we show in several tumor models that although the growth of primary tumors in Batf3-deficient mice, which lack cross-presenting DCs, was not different from primary tumors in wild-type (WT) control mice, Batf3-deficient mice had increased experimental and spontaneous metastasis and poorer survival. The increased metastasis was independent of CD4+ and CD8+ T lymphocytes, but required NK cells and IFNg. Chimeric mice in which Batf3-dependent DCs uniformly lacked the capacity to produce IL12 had metastatic burdens similar..
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Awarded by Bristol-Myers Squibb
Funding Acknowledgements
M.J. Smyth was supported by a National Health and Medical Research Council of Australia (NHMRC) Senior Principal Research Fellowship (1078671) and Program Grant (1013667), and S.L. Nutt was supported by an NHMRC Principal Research Fellowship (1058238) and Program Grant (1054925). E.M. Putz was supported by an Erwin Schroedinger Fellowship of the Austrian Science Fund (J-3635). K.A. Markey is a Queensland Health Junior Clinical Research Fellow. We thank Kate Elder and Liam Town for their technical support with breeding and genotyping of mice. We also thank Fernando Souza-FonsecaGuimaraes and Stuart Olver for their technical help with the cytotoxicity experiments.