Imanishi and Makela (1, 2) first reported that the primary anti-4-hydroxy-3-nitrophenyl acetyi (NP) ~ antibody has a heteroclitic fine specificity in most strains of mice expressing the Igh-1 b allotype, with anti-NP antibodies binding chemical analogues such as 4-hydroxy-5-iodo-3-nitrophenyl acetyl (NIP) with greater affinity than NP itself; the idiotype, termed NP b, was found predominantly expressed along with lambda light chains. Cramer et al. In a previous report, we described the expression of cross-reactive cutaneous sensitivity (CS) responses induced by NP-O-succinimide (NP-O-Su) and elicited by NIP-O-succinimide (NIP-O-Su) in strains of mice possessing the Igh-1 b allotype, but not in strains bearing allotypes Igh-1 c or Igh-1 j (7). The present report extends these observations by analyzing the cross-reactivity of NP-O-Su-induced CS responses in additional inbred strains of mice. Some strains of mice that failed to demonstrate cross-reactive NP-induced DTH responses were able to mount cross-reactive CS responses after NP-O-Su priming, despite the absence of NP b idiotype in these strains.The present report also presents evidence for the existence of at least two T cell subsets within the NP-specific CS effector cell population, at least in the AKR strain: one H-2I-restricted, the other H-2K/D-restricted; each associated with a distinct fine specificity pattern, presumably the manifestation of different receptors on these T cell subpopulations.
Materials and MethodsMice. All mice were either purchased from The Jackson Laboratory, Bar Harbor, Maine, or were bred in the animal facilities at Harvard Medical School, Boston, Mass. Mice were used *