Genetic Control of the Immune Response

Abstract

The influence of immunization with (T,G)-A--L on the frequency and characteristics of [125I] (T,G)-A--L-binding cells (ABC) was investigated in high and low responder mice, whose ability to respond to (T,G)-A--L is under control of an H-2-linked immune response gene, Ir-1. Unimmunized high and low responder mice have about the same number of ABC in spleen and lymph nodes (6–12 ABC/104). However, after immunization with (T,G)-A--L in aqueous solution, ABC in high responders increase to a much greater extent than they do in low responders. By inhibition of ABC with class-specific anti-Ig sera, it was demonstrated that in nonimmune and primed mice antigen is bound to IgM receptors, which is in agreement with the exclusive production of 19S anti-(T,G)-A--L antibody in primed animals. In contrast, after secondary challenge with antigen, ABC in high and low responder mice have mainly IgG receptors, although under the conditions used for immunization, low responders are not able to produce detectable amounts of 7S anti-(T,G)-A--L antibody. From these results and from the evidence that low responders very probably have a T cell defect, it is suggested that the switchover from IgM to IgG precursor cells can be induced by antigen itself, without the action of specific T cells. Furthermore, the failure of marked proliferation of ABC in low responders after antigenic stimulation is explained by the lack of stimulation by specific T cells. By independent methods it has been shown that all ABC detected in this study are B cells. Preliminary experiments indicate that purified peripheral T cells bind antigen, but much less per cell than do B cells.

Nylon adherent antigen-specific rosette-forming T cells.

“…Binding of soluble antigens by T cells has been particularly difficult to demonstrate and was thought to be due to a low site density of antigen-specific receptors in the T-cell membrane (1,2). It is more likely however, that the difficulty in demonstrating binding of soluble antigen by T cells is due to particular temperature and antigen concentration requirements requisite for antigen binding to occur (3,4).…”

Protective antibodies against a sphingomyelinase D from Loxosceles intermedia spider venom elicited in mice with different genetic background

“…Studies from 70s to 80s first showed the interference of HLA in direct the immunoglobulin production and responses to immunization [28][29][30][31][32]. In regard to test the capacity of different HLA in response to rLiD1 we immunized BC and C57 mice and also the transgenic mice with the protein adsorbed in MONTANIDE adjuvant.…”

Immune Response against Hamster Erythrocytes in the Low‐Responder Mouse Strains

“…Dunham et al [5] found that the nonresponder mice to a linear random copolymer (L-Glu60 L-Ala30 L-Tyr10)n (GAT) had the same number of antigen-binding cells as the responder mice, as determined by an autoradiographic study of binding of GAT-125I to spleen cells. Hdmmerling et al [6] also reported that the high-responder and lowresponder mice to a branched, multichain polypeptide(T, G)-A--L had about the same number of antigen-binding cells both in the spleens and lymph nodes. According to Biozzi et al [2], the strain difference in antibody production against sheep erythrocytes (SRBC) between two strains of mice was found to be attributable principally to the difference in doubling times of cells engaged in antibody response rather than to different numbers of antigen-specific lymphocytes initiating the immune response.…”