International Immunology, Vol. 13, No. 4, 459-463,
April 2001
© 2001 Japanese Society for Immunology
NK cells and NKT cells collaborate in host protection from methylcholanthrene-induced fibrosarcoma
Cancer Immunology, Peter MacCallum Cancer Institute, St Andrews Place, East Melbourne, Victoria 8006, Australia
1 Department of Pathology and Immunology, Monash University Medical School, Prahran, Victoria 3181, Australia
Correspondence to: M. Smyth, Cancer Immunology, Peter MacCallum Cancer Institute, Locked Bag 1, A'Beckett Street, Victoria, Australia
NK1.1+ V
14J281+ (NKT) cells can be induced by IL-12 therapy to mediate tumor rejection; however, methylcholanthrene (MCA)-induced fibrosarcoma is the only tumor model described where NKT cells play a natural role in controlling tumor initiation. From our previous study in C57BL/6 mice it remained unclear whether NK cells were also involved in this natural response. Herein, to discriminate the function of NK and NKT cells, we have evaluated fibrosarcoma development in mice deficient in NKT cells, but not NK cells, and mice deficient in NK cells, but not NKT cells. The results indicate that both NK cells and NKT cells are essential and collaborate in natural host immunity against MCA-induced sarcoma. In contrast, sarcoma incidence and growth rate were reduced using IL-12 therapy, this effect was mediated in the absence of T cells (including NKT cells), but not NK cells.
Keywords: immunotherapy, in vivo animal model, NK cell, NKT cell, tumor immunity
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