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The immune response of mice to the synthetic polypeptides (T,G)‐A–L and (H,G)‐A–L is genetically controlled by the Ir‐1 locus. In an attempt to characterize the cell type(s) involved in this control, DNP‐conjugates of (T,G)‐A–L and (H,G)‐A–L were used to study the carrier function of these polypeptides. In adoptive cell transfer experiments carried out in C57BL and C3H mice it was found that in contrast to the respective high responder strain, low responder mice appear to be incapable of recognizing these polypeptides as carriers. This is compatible with the hypothesis that low responders are defective with respect to the specific stimulation of thymus‐dependent lymphocytes by (T,G)‐A–L or (H,G)‐A–L, or to the cooperation of these cells with the precursors of antibody‐producing cells.
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Wrede et al. (1973) studied this question.
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