Antigen- and receptor-driven regulatory mechanisms. III. Induction of delayed type hypersensitivity to azobenzenearsonate with anti-cross-reactive idiotypic antibodies.

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Abstract
Delayed-type hypersensitivity (DTH) to p-azobenzenearsonate (ABA) can be induced in A/J mice with i.v. injection of minute amounts of anti-cross-reactive idiotypic (CRI) antibodies, providing that the animals have been pretreated 2 days earlier with low doses of cyclophosphamide (50 mg/kg). I.v. injection of the F(ab'')2 fragments of the anti-CRI antibodies or s.c. administration with anti-CRI antibodies induces comparable immunity in cyclophosphamide-pretreated and normal nontreated animals. Adoptive transfer experiments indicated that lymph node cells taken from animals sensitized with anti-CRI 4 days earlier can adoptively transfer immunity to naive recipients. Transfer of immunity was mediated by a population of thymus-dependent (T) cells, which express idiotypic structures on their surface. Treatment of effector cells with anti-.theta.-serum or anti-idiotypic antibodies plus complement completely abrogated their ability to transfer immunity. Idiotype-bearing suppressor T cells induced with ABA-coupled spleen cells inhibit the development of ABA-specific DTH induced with anti-CRI antibodies. Genetic analysis revealed that the ability of anti-CRI antibodies to induce ABA-specific DTH was linked to Igh-1 H-chain allotype. Anti-idiotypic antibodies to the major CRI associated with anti-ABA antibodies in A/J mice failed to induce significant immunity in BALB/c mice (H-2d, Igh-1a). They were able to induce significant immunity in C.AL20 mice (H-2d, Igh-1d), which possess a H-chain allotype similar to that of A/J mice.

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