Abstract

The generation and/or expression of suppressor T lymphocytes (Ts) in contact allergy to 2,4-dinitrofluorobenzene (DNFB) is inhibited by treatment of BALB/c mice with C. parvum. It has been described that C. parvum injected intravenously (IV) or intraperitoneally (IP) suppresses lymphocytic responses via activated macrophages. In this investigation we compared Ts and T-effector lymphocytes of delayed hypersensitivity (TDH) inhibition and suppression of mitogen-induced spleen lymphocyte proliferation by C. parvum to find some correlation between these effects of C. parvum. Various times after IP injection of C. parvum BALB/c mice were tolerized (a) by an epicutaneous antigen overload, (b) by 2,4-dinitrobenzene (DNBSO3 IV, (c) by injection of Ts cells from tolerant donors, or (d) sensitized with an optimal dose (15 μl) of DNFB. Suppressor and effector cell generation and/or function was assessed by sensitization (2×0.5% DNFB) and challenge at the right ear or by transfer of spleen cells from the C. parvum-treated or-untreated tolerized donor to the C. parvum-treated or-untreated recipient, followed by sensitization and challenge of the recipient. From the same pool of C. parvum-treated or-untreated animals, spleens were obtained, weights determined, spleen cells prepared, and mitogen (phythemagglutinin or concanavalin A)-induced lymphocyte proliferation measured. The results show that C. parvum-mediated inhibition of Ts generation in the donor mice correlated — although not entirely — with suppression of mitogen-induced lymphocyte proliferation. Inhibition of Ts function in the recipient by C. parvum did not correlate with suppression of spleen lymphocyte proliferation, i.e., Ts function was inhibited up to 1 week only. Lymphocyte proliferation, however, was inhibited up to 3 weeks after C. Parvum injection. Sensitization of mice was inhibited by C. parvum shortly after injection; 1 week after C. parvum injection, no inhibition of contact sensitivity was observed. These results suggest that Ts-cell generation might be suppressed by a similar mechanism as described for suppression of lymphocyte proliferation, i.e., via suppressive factors released from C. parvum-activated macrophages, however, Ts-cell function appears not to be inhibited by this mechanism. T-effector cells of delayed hypersensitivity are very little affected by C. parvum-mediated suppression.

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