[Cancer and immunosuppression : experimental aspects]

The hypothesis that immunodepression favors a carcinogenetic process and thus subsequent tumor development remains controversial in spite of numerous experimental studies. This is due, on one hand, to the difficulty in demonstrating the presence of tumor-associated antigens and, on the other, to the complex immunological mechanisms which lead to the destruction of tumors cells. With respect to immunosurveillance, the present situation can be summarized as follows: the development of virus-induced tumors is under the control of a T-cell dependent system; a T-cell depression (thymectomy, congenital absence of thymus, anti-lymphocytic serum) increases the number of these tumors; chemically induced tumors or spontaneous tumors are under the control of non-specific effectors such as macrophages and NK cells; NK cell deficiency (of congenital origin such as in beige mice) or acquired (chemically induced) increases tumor growth; carcinogens can induce general immunodepression (chemical carcinogenesis) or stimulate specific suppressive cells (U.V. radiation) thus allowing tumors development. The tumors being established, it may itself contribute to an immunodepressive state thus fostering its growth through the activity of: immune complexes; specific or non specific suppressive cells; an increase in the level of alpha 2-globulin immunosuppressive molecules which are present under normal conditions; a release of several factors acting at different levels such as prostaglandin E, anti-inflammatory factors acting on monocytes, etc. The apparition of an antigenic and immunogenic tumor heterogeneity due to development of new clones will also modify host-tumor relationships. The complexity of the immunological mechanisms which are involved in the control of tumor growth may explain the variable results of immune prevention and of the immunotherapy of cancer.