Modulation of suppressor mechanism in allergic contact dermatitis. IV. Selective inhibition of suppressor T-lymphocytes by serum obtained from Corynebacterium parvum treated mice.

We have previously shown that Corynebacterium parvum treatment reduced tolerance induced by intravenous injection of 2,4-dinitrobenzene sulfonic acid (DNBSO3) or by sensitizing BALB/c mice with a supraoptimal dose of 2,4-dinitrofluorobenzene (DNFB). Further analysis by transfer experiments revealed that the generation and/or functional expression of suppressor T-lymphocytes (Ts-cells) was inhibited in both tolerance models. Inhibition of Ts-cells was not entirely correlated with suppression of mitogen induced lymphocyte proliferation mediated by C. parvum activated macrophages. In this investigation we studied the effect of serum obtained at various times after C. parvum injection on tolerance and Ts-cells in DNFB contact allergy. Serum obtained 6 and 24 hr, however, not 72 hr after C.parvum injection inhibited Ts-cells, induced by DNBSO3 and tested by transfer to naive recipients, as efficiently as C. parvum itself. The serum had following characteristics: (1) It inhibited the functional expression of Ts in the recipient animal. (2) It inhibited tolerance induction by an epicutaneous supra-optimal dose of DNFB. (3) It did not inhibit the induction and functional expression of T-effector cells of delayed hypersensitivity (TDH-cells) as shown by transfer experiments. (4) The Ts-inhibitory factor was heat resistant (56 degrees C), not destroyed or lost by dialysis against tris-glycine buffer pH 2 and could not be detected in the serum of NMRI-mice injected 24 hr before with C parvum. (5) The C parvum serum did not significantly increase the spleen weight or suppress mitogen-induced spleen lymphocyte proliferation. The nature of this Ts-cells inhibitory factor is unknown, although the results suggest that cortisone or transfer of bacteria are not responsible. Factors mediating selective inhibition of Ts-cells may be of important regulatory function in delayed type hypersensitivity.