Prevention of primary simian adenovirus type 7 (SA7) tumors in hamsters by adoptive transfer of lymphoid cells: role of different cell types.

Abstract

Malignant neoplasms in general acquire neo-antigens, usually called tumor-specific transplantation antigen (TSTA). Chemically induced tumors usually exhibit antigens unique to each tumor, whereas tumors induced by a virus share a common antigen specific for that virus regardless of the histological type of tumor or host species in which the tumor was induced (1–3). These TSTA invoke an immune response, mainly of cell-mediated type. The immune control or progressive growth of the tumor depends upon many factors including strength of the cellular immune response (degree of sensitization of lymphoid cells), “sneaking through” or appearance of serum blocking factor (1, 3–5), and suppressor cells (6–8). It has generally been accepted that thymus-dependent lymphocytes (T) are primarily responsible for rejection of tumors (9–15). There is considerable evidence that macrophages also contribute an important effector mechanism against tumors (16). Recently, natural killer (NK) cells are also thought to be involved in tumor surveillance (17–19). Most of the studies of effector mechanisms of tumor immunity have been carried out in vitro, using various cytotoxicity assays. To assess the role of in vivo cell-mediated immune responses in tumor immunity, two main approaches usually have been used. One consisted of studying the influence of immuno-suppression (x-irradiation, thymectomy, anti-lymphocyte serum) on the development of tumors (20–24). The alternate approach is to augment cellular immune responses either through non-specific stimulation such as Bacillus Calmette-Guerin (BCG), Corynebacterium parvum (CP), poly I:C, etc. (25–28), or through adoptive transfer of specifically sensitized lymphoid cells (29–31).