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The carcinoembryonic antigen (CEA) modulates effector‐target cell interaction by binding to activated lymphocytes
Author(s) -
Kammerer Robert,
von Kleist Sabine
Publication year - 1996
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19961115)68:4<457::aid-ijc10>3.0.co;2-2
Subject(s) - carcinoembryonic antigen , lymphokine activated killer cell , cytotoxic t cell , cancer research , chemistry , antigen , cell adhesion molecule , effector , cell , immunology , in vitro , biology , medicine , interleukin 21 , cancer , biochemistry
We and others have shown that the carcinoembryonic antigen (CEA) modulates the susceptibility of human colorectal carcinoma cells to cytotoxic lymphocytes. We now demonstrate that the density of the CEA molecules on the tumor cell surface has a determining influence on its protective function. In contrast, CEA released by tumor cells has no protective effect for CEA‐negative cells. To elucidate the responsible mechanism, we analyzed the binding properties of CEA to lymphokine activated killer (LAK) cells. In agreement with our observation that only membrane‐bound CEA provides protection, we found that intercellular contact between LAK cells and CEA‐expressing tumor cells is required for binding of CEA to LAK cells. Using FACScan analysis, we demonstrate the presence of CEA on lymphocytes co‐cultured with CEA‐transfected cells but not after co‐culture with their parental cells and after incubation with soluble CEA. Interestingly, following overnight co‐culture the amount of bound CEA on LAK cells was identical regardless of adherence on tumor cells or loss of contact with tumor cells. This indicates that CEA is released from the tumor cells after binding to LAK cells. Our results suggest that tumor cells can modulate effector cell adhesion by regulating the turnover rate of CEA on the tumor cell membrane. © 1996 Wiley‐Liss, Inc.