The ectopic expression of
Fc gamma RII by PyV transformed 3T3 cells derived from
tumors of long latency has been established. It was suggested that this expression is one of several changes conferring upon the cells an increased capacity for survival. We found that in one case cells expressing a very high level of
Fc gamma RII had also a very high metastatic phenotype as compared to FcR negative cells. Direct evidence that Fc gamma RIIbl functions as a progression factor was provided by transfection experiments. The transfected gene conferred an increased
malignancy and invasive phenotype upon PyV or c-Ha-ras transformed cells. In the present study we tested the possibility that
Fc gamma RII expressing
tumor cells could interfere with the immune system. The following subjects were investigated: 1) The ability of Fc gamma R on the
tumor cells to bind the
ligand and/or release IBF. 2) The effect of a local accumulation of
ligand and/or IBF (assumed to take place in situ in the
tumor) on
Fc gamma RII expressing T cells. It was found that both
tumor-derived receptor positive and beta l transfected PyV transformed cells were capable of binding aggregated mouse
IgG. The binding of bivalent
ligand was followed by an increase in membrane
Fc gamma RII expression. Also both types of cells were capable of releasing IBF. We then tested the possibility that a local accumulation of
IgG within the
tumor could effect Fc gamma R expressing T cells. It was found that aggregated mouse
IgG (as well as IgGl) could stimulate the proliferation of the T cell hybridoma (T2D4) and other
Fc gamma RII expressing T cells. We also found that the expression of beta
Fc gamma RII specific
mRNA peaked at the logarithmic phase of T2D4 cultures, in parallel with their maximal potential to release IBF. Several pathways for interference with the immune system are suggested.