Inhibition of T suppressor cell expression by histamine type 2 (H2) receptor antagonists.
The effect of histamine type 2 (H2) receptor antagonists, cimetidine and ranitidine, on the induction and expression of hapten-specific suppressor T cells was studied. The activity of DNBSO3 -induced suppressor cells was evaluated after adoptive transfer to naive syngeneic recipients. Treatment with cimetidine or ranitidine markedly inhibited suppressor T cell activity in a dose-related manner and enhanced the contact sensitivity response to DNFB. Both H2 antagonists were effective in inhibiting the expression and, to a lesser extent, the induction of suppressor T cells. In contrast, norburimamide , a non-H2 antagonist structurally related to cimetidine, was inactive. The relevance of these findings to the clinical observation of cimetidine-induced reversal of acquired tolerance to dinitrochlorobenzene in anergic patients is discussed.
D000818:Animals; D001557:Benzenesulfonates / Q000276:immunology; D002927:Cimetidine / Q000494:pharmacology*; D004139:Dinitrofluorobenzene / Q000276:immunology; D000939:Epitopes; D007108:Immune Tolerance; D007116:Immunization, Passive; D007166:Immunosuppressive Agents / Q000494:pharmacology*; D008213:Lymphocyte Activation / Q000187:drug effects*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D011899:Ranitidine / Q000494:pharmacology*; D050378:T-Lymphocytes, Regulatory / Q000187:drug effects* / Q000276:immunology / Q000637:transplantation
D001557:Benzenesulfonates; D000939:Epitopes; D007166:Immunosuppressive Agents; C001073:2,4-dinitrobenzenesulfonic acid; D002927:Cimetidine; D011899:Ranitidine; D004139:Dinitrofluorobenzene