Role of T suppressor cells in the cycling of the immune response against a murine fibrosarcoma

Abstract

Antitumor immunity against a fibrosarcoma in C57BL/6 mice was obtained by means of a semi-allogenic somatic hybrid cell derived from the fusion of this C57BL/6 fibrosarcoma (MCB6-1) and A9 cells of C3H origin. In a Winn assay, this immunity could be transferred by T lymphocytes to normal C57BL/6 recipient mice during an early and a late phase after immunization. There appeared to be a transient non-responsive period during which no immunity could be transferred. Injection of cyclophosphamide (CY) into mice before immunization increased the level of immunity during this period, and reconstitution of animals with normal spleen cells abolished the effect of CY. During the non-responsive period, suppressor cells were demonstrated in the spleen: the i.v. transfer of these suppressor cells to normal mice significantly inhibited the induction of antitumor immunity; the suppressive effect was transferred by T lymphocytes of the Lyt-2+ phenotype. No suppressive effect on antitumor protection was observed when suppressor cells were transferred simultaneously with immune T lymphocytes in the Winn assay. From these findings, it appears that T-suppressor cells regulate the antitumor response, interfering with the afferent (induction) arm of the immune response.

Temporal changes of suppressor T lymphocytes and cytotoxic T lymphocytes in syngeneic murine malignant gliomas

“…Drebin et al, however, demonstrated that Lyt-1-.2.3 ÷ Ts are generated as early as 24 h after the s.c. tumor inoculation (33). Furthermore, it has been demonstrated by several authors (34)(35)(36)(37)(38)(39)(40) that Ts are largely Lyt-2 cells, although they carry small numbers of Lyt-1 determinants. Presumably, suppression by Lyt-1-.2.3 + Ts is an example of T-cell-mediated unresponsiveness (passive suppression), in contrast to active T-cell-mediated suppression.…”

Histocompatibility Antigens on Murine Tumors

“…For example, the expression of H-2D, in association with tumor-associated target antigens, might bx&rt a regulatory effect on the specific immune response against the tumor. This might occur through interactions with suppressive immune components such as suppressor T cells (49) or by induction of CTL's capable of recognizing T-cell receptor structures on CTL's specific for the tumor (50). Such specific immune suppression could explain the lack of immunogenicity associated with these subclones (51).…”