Abstract
A novel tumour system has been used to study the effect of natural killer cells on tumour growth by using agents which modify natural killer cell activity. The tumour cells are hybridoma cells which secrete antibody specific for red blood cells so that tumour growth can be quantitated by a haemolytic plaque assay. Spleen-seeking variants have been derived from original hybrids which are sensitive to natural killer cells. Treatment of mice with polyinosinic-polycytidylic acid substantially enhanced natural killer cell activity and correlated closely with a reduction in the growth of the hybridoma tumour cells in the spleen and life extension. Conversely, a single injection of anti-asialo GM, antibody resulted in a substantial increase in the number of plaque forming splenic tumour cells and virtual elimination of natural killer cell activity. These data demonstrate the important role of natural killer cells in constraining the growth of a tumour of B cell origin and establishes the usefulness of this tumour model in studying the biology of effects on tumour growth.
Highlights
In order to establish that the hybridoma tumour cells were killed by cytotoxic cells occurring naturally in fresh splcen cells, spleen cell suspensions from normal and poly I-C treated mice were tested for their ability to kill HeC3 cells in a 4 h 51Cr release assay
When the tumour plaque-forming cells (PFC) were measured there was an increase in the mean number of tumour cells with 5.6+1.8 x 105 PFC in the treated compared to 3.2 +2.3 x 104 PFC in control mice (P
Blood borne metastases are likely targets for NK cell activity, it is generally accepted that the overall 'level' of NK cells may not reflect the concentration in crucial sites for potential control of tumour growth (Moore, 1985)
Summary
Male and female, (BALB/c x DBA/2) F1 H-2d (designated CDF1), CBA/J H-2k, DBA/2 H-2d and (CBA x DBA)F1 mice aged 9-12 weeks were obtained from the mouse colony in the School of Medicine University of Auckland They were age and sex matched for each experiment. The hybridomas were passaged several times in young BALB/c mice and two variant sublines were derived designated BSp and HeSp (Ezaki & Marbrook, 1985). These two tumourigenic variants grew as spleen colonies in normal adult CDF1 and BALB/c mice, but would not grow in DBA/2, CBA/J or (CBAxDBA)F1 mice.
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