Abstract
The results of this study of allogeneic restriction of passively transferred delayed sensitivity to Listeria antigens serve to illustrate the complexity of in vivo models. They show that the H-2 restriction observed when delayed-type hypersensitivity was transferred between H-2-congenic strains was no more severe than the restriction observed when delayed-type hypersensitivity was transferred between parental and F1 mice and between different strains sharing the same H-2 haplotype. It is obvious that genes, in addition to those of the H-2 locus, can be responsible for allogeneic restriction in vivo.
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