Abstract
Dinitrophenylated macrophages are efficient inducers of contact sensitivity and of tolerance to dinitrochlorobenzene, depending on the mode of application. Contact sensitivity induced by an intradermal injection of DNP-M phi is genetically restricted, whereas tolerance induced by an intravenous injection is, in guinea pigs, not under control. This tolerance is complete in the majority of animals, but is reversed by DNCB in Freund's complete adjuvant and prevented by pretreatment with cyclophosphamide. Tolerance induced by an intravenous injection of the unconjugated hapten is not reversed by DNCB in FCA, but is abrogated by an intradermal injection of DNP-M phi. This abrogation does not occur, however, when DNCB in FCA is applied simultaneously with the DNP-M phi. In further experiments, it is demonstrated that the genetic restriction of induction of contact sensitivity by DNP-M phi is on the level of antigen recognition and is not due to the nonidentity of the Ia structures on macrohages used for induction and the Ia structures involved in elicitation of contact sensitivity.
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