EPITOPE MASKING OF RAT ESOPHAGEAL-CARCINOMA TUMOR-ASSOCIATED ANTIGEN BY CERTAIN COEXISTING GLYCOLIPID AND PHOSPHOLIPID MOLECULES - A POTENTIAL MECHANISM FOR TUMOR-CELL ESCAPE FROM THE HOST IMMUNE-RESPONSES

Citation
Rj. Jamasbi et al., EPITOPE MASKING OF RAT ESOPHAGEAL-CARCINOMA TUMOR-ASSOCIATED ANTIGEN BY CERTAIN COEXISTING GLYCOLIPID AND PHOSPHOLIPID MOLECULES - A POTENTIAL MECHANISM FOR TUMOR-CELL ESCAPE FROM THE HOST IMMUNE-RESPONSES, Cancer immunology and immunotherapy, 38(2), 1994, pp. 99-106
Citations number
36
Categorie Soggetti
Immunology,Oncology
ISSN journal
03407004
Volume
38
Issue
2
Year of publication
1994
Pages
99 - 106
Database
ISI
SICI code
0340-7004(1994)38:2<99:EMORET>2.0.ZU;2-1
Abstract
A monoclonal antibody (mAb-5G) produced against a tumorigenic rat esop hageal cell line, B2T, was shown to react specifically with a unique g lycolipid antigen expressed on the cell surface of tumorigenic and cer tain non-tumorigenic, immortalized rat esophageal cell lines [Cancer I mmunol Immunother 36: 94 (1993)]. In enzyme linked immunosorbent assay experiments, mAb-5G reacted with crude lipid extracts prepared from B 2T cells cultured in vitro, but showed very little reactivity with cru de lipid extracts prepared from the same cell line passaged once in vi vo, unless the antigen was separated from other lipid components by co lumn or thin-layer chromatography (TLC). When a secondary tissue-cultu re cell line was established from the above B2T tumor tissues and seri ally subcultured in vitro, the percentage of positively stained cells was increased significantly in immunofluorescence assay. It was also d emonstrated that the amount of extractable antigen was increased as th e cells were subcultured in vitro up to passage 15, and stabilized the reafter. These results indicate the presence of certain lipid componen ts in crude lipid extracts from B2T cells grown in vivo that are capab le of interfering with antigen-antibody binding. On TLC plates, these interfering lipids were identified as phosphatidylcholine, phosphatidy lserine, sphingomyelin and gangliosides. The interfering lipids did no t bind the antibody, rather they appeared to interfere with antigen ac cessibility. These lipid substances may modify tumor cell surface anti gen(s), thus protecting the tumor cells from host immune destruction.