Possibilities of Interference with the Immune System of Tumor Bearers by Non-Lymphoid FcγRII Expressing Tumor Cells

Maya Ran*, Adit Ben Baruch Langer, Ilan Eliassi, Ofrah Gohar, Bosmat Gonen, Serge Gradsztajn, Wolf H. Fridman, Jean Luc Teillaud, Isaac Witz

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

6 Scopus citations

Abstract

The ectopic expression of FcγRII 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 FcγRII had also a very high metastatic phenotype as compared to FcR negative cells. Direct evidence that FcγRIIbl 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 FcγRII expressing tumor cells could interfere with the immune system. The following subjects were investigated: 1) The ability of FcγR 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 FcγRII expressing T cells. It was found that both tumor-derived receptor positive and βl transfected Py V transformed cells were capable of binding aggregated mouse IgG. The binding of bivalent ligand was followed by an increase in membrane FcγRII 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 FcγR expressing T cells. It was found that aggregated mouse IgG (as well as IgGI) could stimulate the proliferation of the T cell hybridoma (T2D4) and other FcγRII expressing T cells. We also found that the expression of βFcγRII 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.

Original languageEnglish
Pages (from-to)415-425
Number of pages11
JournalImmunobiology
Volume185
Issue number2-4
DOIs
StatePublished - 1992

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