Anti-idiotypic antibodies (anti-Id) that contain an internal image component that mimics the surface antigen of hepatitis B virus (HBsAg) were used to immunize chimpanzees. Four injections of the rabbit anti-Id preparation elicited an antibody response to HBsAg (anti-HBs). The antibody specificity appeared to be against the anti-Id, since the anti-Id immunogen was shown to bind the chimpanzee anti-HBs. Two chimpanzees immunized with the anti-Id, along with two control animals that were either untreated or received a nonimmune rabbit immunoglobulin G preparation, were challenged with infectious hepatitis B virus. Both control chimpanzees developed clinical and serological characteristics consistent with an active hepatitis B virus infection, whereas the two anti-Id treated chimpanzees were protected from infection. Since chimpanzees provide a relevant model of a human response to hepatitis B virus immunization and infection, these results indicate that anti-Id preparations such as that described here might be candidates for vaccines against human diseases.

https://science.sciencemag.org/content/sci/232/4747/220.full.pdf

Anti-idiotypic antibody vaccine for type B viral hepatitis in chimpanzees.

Idiotopes are markers on the variable domains of antigen-specific immunological receptors recognized by anti-idiotypic antibodies or T cells. Therefore, a given antibody or T cell receptor can be identified on the basis of a characteristic idiotypic pattern. The structural correlates for idiotopes on antibodies have been studied by competitive binding assays, electron microscopy, site-directed mutagenesis, and X-ray crystallography. Immunoglobulin idiotopes, recognized by antiidiotypic antibodies, can involve amino acid residues from several hypervariable or framework regions and from either or both of the heavy and light chain variable domains. Recent studies suggest that it may be possible to exploit structural knowledge of idiotopes and anti-idiotopes for the design of new ligands for immunological or other cell surface receptors. In one instance, it has been possible to use the inferred structural features of an anti-idiotope, which mimics a viral protein, to design a small organic molecule with functional properties approximating those of the antigen and the native anti-idiotope. An alternative strategy being explored for creating new vaccines or therapeutic agents involves engineering an amino acid sequence, corresponding to a segment of a selected nominal antigen, into an immunoglobulin variable domain.

Idiotypes: structure and immunogenicity.

In this study, we assessed the proliferative response of T cells from mice chronically infected with Trypanosoma cruzi to actin, myosin, or T. cruzi soluble antigen (SA). We report here that CD4+ T cells from mice chronically infected with T. cruzi proliferated in response to myosin but not to actin, whereas cells from naive mice did not proliferate against any of the antigens tested. Antisera raised against myosin- or SA-activated T cells specifically inhibited respectively, the myosin or SA in vitro proliferative response, whereas the response to unrelated antigen remained unimpaired. Sera from chronically infected mice failed to show any significant inhibitory activity. The above findings suggest that autoreactive and T. cruzi-reactive T cells belong to different, perhaps nonoverlapping, compartments of the immune cell repertoire of mice chronically infected with T. cruzi. The failure of infected mice to trigger the suppressive mechanisms described here might be the primary immune defect leading to breakdown of self-tolerance and unopposed, perhaps tissue-damaging, autoimmunity in experimental Chagas' disease.

Autoimmunity in Chagas' disease: specific inhibition of reactivity of CD4+ T cells against myosin in mice chronically infected with Trypanosoma cruzi.

Mice were infected with the intracellular bacterium, Listeria monocytogenes, and T cell clones from spleens, lymph nodes and peritoneal exudates were established. The capacity of L3T4+, Lyt2- T-cell clones to specifically lyse L. monocytogenes-infected macrophages was analyzed. As a source of target cells, bone marrow macrophages (BMM phi) after 9 days of culture in hydrophobic teflon bags were used. These BMM phi were totally Ia-; however, significant Ia-expression could be induced by interferon-gamma (IFN-gamma). IFN-gamma-stimulated BMM phi, after priming with live or killed L. monocytogenes organisms were effectively lysed by the vast majority of L3T4+ T cell clones. In the absence of either IFN-gamma stimulation or antigen priming, no lysis occurred. Cytolysis was demonstrable in a conventional 4-h 51Cr-release assay and in an 18-h neutral red uptake assay and was antigen specific and class II restricted. Native T cells from L. monocytogenes-infected mice failed to lyse stimulated, L. monocytogenes-primed BMM phi and gained their cytolytic activity after antigenic restimulation in vitro. These data demonstrate that L. monocytogenes-specific L3T4+ T cells could lyse M phi presenting listerial antigens provided that Ia antigen expression had been induced. L3T4+ T cell clones produced IFN-phi after restimulation with antigen plus accessory cells in vitro and IFN-gamma secretion could be increased by costimulation with recombinant IL 2. These T cell clones conferred significant protection upon recipient mice which was more pronounced in the liver. The possible relevance of lysis by L3T4+ T cells of infected M phi to protection against and pathogenesis of intracellular bacterial infections is discussed.

Specific lysis of Listeria monocytogenes-infected macrophages by class II-restricted L3T4+ T cells.

https://www.cell.com/imto/pdf/0167-5699(87)90827-9.pdf

The immunology of new generation vaccines

The T cell clone 26.1.1, which confers specific protection against the intracellular bacterium Listeria monocytogenes, was fused to BW 5147. The resulting T cell hybridoma, TLm1, could be stimulated to secret interleukin 2 by antigen plus accessory cells or concanavalin A. Stimulation was specific for an epitope expressed by L. monocytogenes EGD but not ATCC 19114 and was H-2I-A restricted. Antisera against TLm1 were raised in syngeneic mice and tested for their capacity to block TLm1 responses. Two antisera were identified that blocked antigen but not concanavalin A stimulation of TLm1 and did not affect antigen stimulation of similar but not identical L. monocytogenes-specific T cell hybridomas. Hence, these antisera had clonotypic activity. When these antisera were administered subcutaneously in complete Freund's adjuvant, mice were protected against a subsequent L. monocytogenes infection. Protection was antigen specific and H-2 nonrestricted. These findings suggest the feasibility of clonotypic antibodies for vaccination against intracellular bacterial infections.

Vaccination against the intracellular bacterium Listeria monocytogenes with a clonotypic antiserum.

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Vaccination against the intracellular bacterium Listeria monocytogenes with a clonotypic antiserum.