[Fas mediated apoptosis inhibited by human bcl-2 gene in lymphoma cell line Jurkat].
OBJECTIVE
To understand the mechanism of bcl-2 gene in escaping the immune surveillance in the development of lymphoma.


METHODS
A recombinant retroviral vector pLXSN-bcl-2 was constructed by cloning bcl-2 cDNA into the replication defective retroviral vector pLXSN, and transferred to packaging cell line PA317 by electroporation. The G418 resistant colonies were selected, and the supernatants of the colony cultures were used to infect the human lymphoma cell line Jurkat. Cells in G418 resistant Jurkat colonies were characterized by immunohistochemistry. Anti-Fas monoclonal antibody (McAb) was applied to Jurkat cells for inducing apoptosis which mimicked the cytotoxic activity of T lymphocyte.


RESULTS
Expression of bcl-2 in pLXSN-bcl-2 transfected Jurkat cell (Jurkat-bcl-2) increased, while there was no change of Fas gene expression. Apoptosis was blocked in Jurkat-bcl-2 by anti-Fas McAb treatment.


CONCLUSIONS
Overexpression of bcl-2 in lymphoma cell line could inhibit cell apoptosis induced by anti Fas McAb, suggesting that overexpression of bcl-2 is one of the mechanisms in escaping immune surveillance in the development of lymphoma.
Tumor Immunology and Gene Therapy Center, Eastern Institute of Hepatobiliary Surgery, Shanghai 200433.
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D017209:Apoptosis; D053222:Fas Ligand Protein; D015870:Gene Expression; D019254:Genes, bcl-2; D006801:Humans; D019169:Jurkat Cells; D008562:Membrane Glycoproteins / Q000276:immunology*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000096:biosynthesis*; D014162:Transfection; D019014:fas Receptor / Q000276:immunology*
C505661:FASLG protein, human; D053222:Fas Ligand Protein; D008562:Membrane Glycoproteins; D019253:Proto-Oncogene Proteins c-bcl-2; D019014:fas Receptor