NK cells and NKT cells collaborate in host protection from methylcholanthrene-induced fibrosarcoma
Author(s) -
Mark J. Smyth,
Nadine Y. Crowe,
Dale I. Godfrey
Publication year - 2001
Publication title -
international immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.86
H-Index - 134
eISSN - 1460-2377
pISSN - 0953-8178
DOI - 10.1093/intimm/13.4.459
Subject(s) - natural killer t cell , fibrosarcoma , methylcholanthrene , interleukin 12 , biology , immunology , immune system , cancer research , interleukin 21 , microbiology and biotechnology , t cell , cytotoxic t cell , in vitro , carcinogen , biochemistry , genetics
NK1.1(+) V(alpha)14J(alpha)281(+) (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.
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