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Multiple deficiencies underlie NK cell inactivity in lymphotoxin-alpha gene-targeted mice
M J Smyth1, R W Johnstone, E Cretney
1Cellular Cytotoxicity Laboratory, The Austin Research Institute, Heidelberg, Victoria, Australia. m.smyth@ari.unimelb.edu.au
Abstract:
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-alpha-deficient mice. Analysis of LT-alpha-deficient mice revealed that the absolute number of alphabetaTCR- 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 alphabetaTCR- NK1.1+ cells, as determined by their lytic capacity and perforin expression, was reduced 1.5- to 3-fold in LT-alpha-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-alpha-deficient mice.