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Gene-Targeted Mice1
*
Cellular Cytotoxicity Laboratory, The Austin Research Institute, Heidelberg, Victoria, Australia;
DNAX Research Institute of Molecular and Cellular Biology, Inc., Palo Alto, CA 94304;
Centenary Institute of Cancer Medicine and Cell Biology, Royal Prince Alfred Hospital, Sydney, New South Wales, Australia; and
Institut fuer Klinische Mikrobiologie, Immunologie und Hygiene, Erlangen, Germany
We have evaluated the NK cell antitumor activity in lymphotoxin
(LT)-deficient mice. Both NK cell-mediated tumor rejection and
protection from experimental metastases were significantly compromised
in LT-
-deficient mice. Analysis of LT--deficient mice revealed
that the absolute number of 
TCR- NK1.1+
NK cells was reduced in bone marrow and thymus, but with overall
proportional decreases in other hemopoietic organs. In addition, the
antitumor potential of TCR- NK1.1+
cells, as determined by their lytic capacity and perforin expression,
was reduced 1.5- to 3-fold in LT--deficient mice, as compared with
wild-type mice. Combined defects in NK cell development and effector
function contribute to compromised NK cell antitumor function in
LT--deficient mice.
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