The site of action of the H‐2 linked gene regulating the ability of mice to be sensitized to transfer delayed‐type hypersensitivity was studied using radiation bone marrow chimeras. Lethally irradiated (non‐responder × responder) F1 were reconstituted with bone marrow cells of both parents. Cells of chimeras immunized with limiting doses of ovalbumin responded as did the parental strains. These results suggest that the gene regulating delayed type hypersensitivity is expressed at the level of the delayed‐type hypersensitivity effector cells or that restrictions exits on the collaboration of the helper cells for DTH effectors (which differ at several loci including the major histocompatibility complex).
|Original language||English (US)|
|Number of pages||5|
|Journal||Scandinavian Journal of Immunology|
|State||Published - Sep 1981|
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