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Genetic Control of the Immune Response: the Effect of Non-H-2 Linked Genes on Antibody Production¹

From the Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115

Abstract

In mice genetic control of the ability to form an immune response to the random terpolymer of glu⁶⁰, ala³⁰, tyr¹⁰ (GAT) is regulated by an Ir gene which maps between the K and Ss-Slp region of the H-2 complex. Several responder mouse strains were immunized with limiting doses of GAT. All responder strains produced GAT antibody after immunization with 1 µg, but not with 0.1 µg GAT. Although all responder strains responded to the same limiting doses of antigen, the serum concentrations of anti-GAT antibodies varied considerably among strains. Thus A, A.By and (B10 x A)F₁ mice demonstrated at least 10-fold higher GAT-binding capacities than B10 or B10.A mice. This dominant non-H-2 linked quantitative trait reflects differences in the concentration of specific antibody since anti-GAT antibodies from A and B10 mice were shown to have similar binding affinities, and inhibition studies with the copolymers GT and GA indicated that both the A and B10 antisera also had similar specificity. Measurements of antibody concentration have shown that sera from A strain mice contained 15-fold more specific antibody than sera from B10 animals. In addition, plaque assays demonstrated more antibody-forming cells in A strain animals.

Genetic analysis demonstrated that these strain differences were under multigenic control. One of the genetic components was shown to be linked closely with the heavy chain allotype loci.

Footnotes

¹ This investigation was supported by Grants AI-09920 and AI-00387 from the National Institutes of Health, United States Public Health Service.

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