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Genetic control of immune response to the H-2Dk private specificity, H-2.32. I. Low responsiveness of the B10 congenic mice to the H-2.32 determinant.

A variety of congenic resistant strains of mice sharing the B10 background have been examined for humoral responsiveness to the H-2D region private specificity H-2.32. All of these strains were found to produce little or no anti-H-2.32 antibody, confirming previous indications that the B10 background is defective with respect to this response (1). However, both strain B10 ( H-2 b ) and strain B10.D2 ( H-2 d ) did produce reasonable titers of antibodies reactive with public H-2D region specificities of H-2 k . In the case of B10.D2, this response could be shown to be due to a response to the D region product itself rather than a cross-reaction with public specificities shared in both K and D regions. By using sera to public and private H-2D k specificities sequentially to precipitate radiolabeled solubilized H-2 antigen preparations, both private and public specificities were shown to be present on the same molecules. Thus, the failure of B10 background mice to respond to the private specificity H-2.32 appears to be peculiar to this specificity and not to all specificities on the H-2D k molecule. Analysis of (AKR.M × B10.AKM)F 1 × B10.AKM backcross mice revealed that the magnitude of the antibody response to H-2 d antigens did not correlate with that of the anti-H-2.32 response, indicating the specific nature of the anti-H-2.32 low responsiveness of B10 congenic mice.