Abstract
In the present paper it is shown that both induction and elicitation of 2,4-dinitrochlorobenzene-contact sensitivity in guinea pigs are genetically controlled. This genetical control is operating by two somehow different mechanisms. The recognition of hapten on allogeneic macrophages during the inductive phase is suppressed by the allogeneic response against these macrophages whereas the elicitation upon transfer of syngeneically primed lymphocytes is limited by the identity of at least some components of the major histocompatibility complex. This nonidentity contradicts the rule of carrier specificity, which is a requirement for all delayed type hypersensitivity reactions. Furthermore, the presentation of haptens to primed cells is less restricted than presentation of protein antigens.