We have previously shown that cross-reactive sensitivity (CS) responses induced by 4-hydroxy-3-nitrophenyl acetyl-O-succinimide (NP-O-Su) and elicited by its 5-iodo analogue, 4-hydroxy-5-iodo-3-nitrophenyl acetyl-O-succinimide were observed in strains of mice possessing the Igh-1b allotype, but not in strains bearing allotypes Igh-1c or Igh-1j. These CS responses are mediated by T cells and can be transferred to naive recipients that are homologous at either the H-2K, H-2I, or H-2D regions of the major histocompatibility complex. We now extend our analysis of cross-reactive 4-hydroxy-3-nitrophenyl-acetyl (NP)-induced CS responses to inbred strains of mice expressing additional Igh-1 allotypes. In contrast to NP-induced delayed-type hypersensitivity responses, which only display 4-hydroxy-5-iodo-3-nitrophenyl acetyl (NIP) cross-reactivity in Igh-1b-bearing mice, cross-reactive CS responses can also be elicited in NP-primed mice carrying the Igh-1d, Igh-1e, or Igh-1f allotypes. Moreover, cross-reactive NP-induced CS responses could be transferred by NP-O-Su-primed lymph node cells from the AKR (Igh-1d) strain, into naive recipients homologous at the H-2D region, but only non-cross-reactive NP responses could be transferred into strains homologous at the H-2I region. Furthermore, the lack of cross-reactivity in the Igh-1j-bearing C3H strain was not the result of an inability of these mice to recognize NP in association with H-2K/D products, because NP-O-Su-primed cells from C3H donors transferred NP-specific CS responses into both H-2D and H02I homologous recipients. The results are discussed with respect to the nature of the T cell receptors that control NP responses.

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