In vivo acquisition of Fc gamma RII expression on polyoma virus-transformed cells derived from tumors of long latency.
BALB/c 3T3 cells transformed in vitro with polyoma virus were cloned and passaged once in syngeneic mice. Resulting tumors from each clone were explanted and recultured. Expression of receptor for Fc of IgG (Fc gamma RII) in the original in vitro maintained clones and in cells derived from tumors elicited by the respective cells was measured at the protein level as well as at the mRNA level. Clones were assayed in pairs. The ancestor in vitro maintained clones [designated cultured cells (C)] were compared with cells derived from the same clones after a single passage in vivo followed by explantation and reculturing [designated cultured-tumor-cultured cells (CTC)]. C cells of any of the tested clones did not express Fc gamma RII. On the other hand, certain CTC cells were positive. The Fc gamma RII-positive cells were derived from tumors appearing after a long precancer latency period (greater than 140 days). CTC cells derived from tumors that appeared after shorter latency periods (less than 80 days) were Fc gamma RII negative. These results were obtained both by using radioimmunoassay and monoclonal antibodies against mouse Fc gamma RII as well as by Northern blot analysis using the Fc gamma RII complementary DNA probe. The involvement of macrophages as the Fc gamma RII-expressing cells in CTC cells was excluded. Fc gamma RII expression was down-regulated in CTC cells as a function of time following their explantation into culture. Fc gamma RII expression could be up-regulated in these cells and induced on C cells by maintaining the cultured cells in the presence of normal mouse serum or recombinant interferon. We also tested the expression of Fc gamma RII on CTC cells following their inoculation into syngeneic mice for a second time (CTCx2 cells). The results showed a positive correlation between Fc gamma RII expression in the inoculated ancestor CTC cells and on the CTCx2 cell progeny.
Ran
M
M
Department of Microbiology, George S. Wise Faculty of Life Sciences, Tel Aviv University, Israel.
Katz
B
B
Kimchi
N
N
Halachmi
E
E
Teillaud
J L
JL
Even
J
J
Berko-Flint
Y
Y
Atlas
E
E
Fridman
W H
WH
Witz
I P
IP
D000818:Animals; D000943:Antigens, Differentiation / Q000032:analysis / Q000235:genetics*; D014408:Biomarkers, Tumor / Q000032:analysis; D002460:Cell Line; D002462:Cell Membrane / Q000276:immunology; D002471:Cell Transformation, Neoplastic; D002999:Clone Cells; D007074:Immunoglobulin G / Q000378:metabolism; D008264:Macrophages / Q000276:immunology; D051379:Mice; D008807:Mice, Inbred BALB C; D009368:Neoplasm Transplantation; D009374:Neoplasms, Experimental / Q000235:genetics* / Q000276:immunology / Q000473:pathology; D011120:Polyomavirus / Q000235:genetics*; D012334:RNA, Neoplasm / Q000235:genetics; D011961:Receptors, Fc / Q000032:analysis / Q000235:genetics*; D017452:Receptors, IgG
D000943:Antigens, Differentiation; D014408:Biomarkers, Tumor; D007074:Immunoglobulin G; D012334:RNA, Neoplasm; D011961:Receptors, Fc; D017452:Receptors, IgG