M.S.

Glucocorticosteroids are drugs commonly used to suppress immune or inflammatory responses. The present study was done to evaluate the influence of glucocorticoids on immunity in fibrosarcoma-bearing mice. Effects of hydrocortisone-21-sodium succinate (HCS) on mitogen-induced lymphocyte proliferation were assessed. T cells from nontumor-bearing mice showed a 2-fold suppression of phytohemagglutinin (PHA) responsiveness with the addition of 0.1 µg HCS. However, T cells from mice with 3-4 week tumors did not demonstrate as great a suppression, if any. Kinetic studies during tumor growth demonstrated a decrease in HCS suppression of mitogen-induced DNA synthesis at 8-10 days post-tumor cell inoculation. RCS-treated cells from mice with 3-4 week tumors had a 2- fold increase in blastogenesis over untreated PHA controls. The role of macrophages and their involvement in the steroid sensitivity of the PHA response is unclear. Evidence reported here indicated that macrophages may be involved as mediators of steroid sensitivity and may therefore limit the extent of their suppressive and/or enhancing activity. In vivo administration of methylprednisolone acetate (MPA) demonstrated that steroids can interfere with the growth and progression of fibrosarcomas in their syngenic BALB/c hosts. The strongest delay in tumor appearance was observed when the steroid was administered 4-7 days post-tumor cell inoculation. It is assumed that after tumor cell inoculation, precursor cells of both suppressor and cytotoxic lymphocytes were entering a proliferative stage to form mature cells. These studies indicated that steroid suppression was directed against a suppressor T cell and possibly acts by preventing its differentiation. It is thought that this suppressor cell acts by inhibiting the lytic function of effector T cells. Thus, by eliminating suppressor T cells, the immune response is capable of eliciting strong anti-tumor immunity. / M.S.