Transferable suppression and intrinsic unresponsiveness in delayed-type hypersensitivity to sheep red blood cells of mice: two distinct mechanisms?
In mice rendered unresponsive in DTH by the i.v. infection of 10(9) SRBC, two forms of specific unresponsiveness could be distinguished, referred to as intrinsic unresponsiveness and suppression. Suppression could be transferred by splenic T cells. It was short-lived and sensitive to cyclophosphamide (Cy, 100 mg/kg i.v.) given after sensitization. On the other hand, intrinsic unresponsiveness was not transferable by either serum or spleen cells. It was long-lived and resistant to Cy (200 mg/kg i.v.) given after sensitization. Induction of both transferable suppression and intrinsic unresponsiveness depended on Cy-sensitive (200 mg/kg i.v.) precursors. Since no evidence for clonal deletion could be obtained, it is suggested that unresponsiveness in general is mediated by complex cellular interactions which are readily perturbed in transfer experiments. In this way, cell recipients would end up possessing incomplete regulatory circuits, intact circuits still being present in donor animals.
D000818:Animals; D003520:Cyclophosphamide / Q000494:pharmacology; D004912:Erythrocytes / Q000276:immunology*; D005260:Female; D006968:Hypersensitivity, Delayed / Q000276:immunology*; D007108:Immune Tolerance / Q000187:drug effects; D007165:Immunosuppression Therapy; D008297:Male; D051379:Mice; D012756:Sheep; D013601:T-Lymphocytes / Q000637:transplantation; D013997:Time Factors
D003520:Cyclophosphamide