Hapten-specific responses to the phenyltrimethyl-amino hapten.I. Evidence for idiotype-anti-idiotype interactions in delayed-type hypersensitivity in mice

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Abstract
The delayed‐type hypersensitivity (DTH) reaction to the phenyltrimethylamino (TMA) hapten in mice has been investigated. TMA‐derivatized syngeneic spleen cells (TMA‐SC) administered S.C. in several strains of mice consistently evoked DTH reactivity, as measured by footpad swelling after challenge with the diazonium salt of TMA. DTH could be induced by low levels of anti‐idiotypic antisera (anti‐Id) in lieu of antigen. The DTH reaction induced by either mode was hapten‐specific, could be transferred into naive recipients by viable lymph node cells but not with serum from immune mice and was not influenced by cyclophoshamide pretreatment. Unlike TMA‐SC which induced DTH in all of the strains of mice tested, anti‐Id induced DTH only in strains of the Igh‐1e allotype. Positive DTH reactions were induced by anti‐Id in the C57.Ige strain (H‐2b, Igh‐1e) but not in its allotype‐congenic partner C57BL/6J (H‐2b, Igh‐lb). Interestingly, this reaction could be suppressed if relatively high amounts of anti‐Id were inoculated i.v. just prior to antigen challenge. In addition, the administration of anti‐Id 1 h prior to antigen challenge in TMA‐SC‐sensitized mice significantly blocked the DTH reaction only in the Igh‐1e strains. These results demonstrate that the induction and abrogation of TMA‐specific DTH by anti‐Id is linked to the IgCH locus.

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