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  • Title: Immune response to the p-azobenzenearsonate-L-glutamic acid60-L-alanine30-L-tyrosine10 (GAT) conjugate. III. Mechanisms of Ir gene-controlled phenotype conversion.
    Author: Flores de Castaneda M, Regnier D, Hermier B, Dubert JM, Seman M.
    Journal: Eur J Immunol; 1984 Oct; 14(10):943-50. PubMed ID: 6237921.
    Abstract:
    Immunization of GT (random copolymer of L-glutamic acid51-L-tyrosine49) nonresponder animals with p-azobenzenearsonate (ABA) GT conjugates elicits an antibody response to both ABA and GT epitopes which is induced by ABA-specific T helper cells. Expression of these hapten-specific helpers is under the control of an I region gene which also regulates the proliferative T cell response to ABA. Conversion of the unresponsive phenotype to GT is, therefore, dependent on the ABA Ir gene and escapes the influence of the GT-specific I region-controlled suppressive pathway. Studies on the influence of ABA/polymer coupling ratio on T and B cell responses suggest that ABA-specific T cells, like conventional carrier-specific helpers, require linked interactions with B lymphocytes to provide helper signals. GAT (terpolymer of L-glutamic acid60-L-alanine30-L-tyrosine10) nonresponder animals immunized with ABA-GAT conjugates also develop an antibody response to ABA which is induced by ABA-specific T helper cells. Comparison of antibody affinity, specificity, isotypes and idiotypes in different mouse strains demonstrates that hapten-specific helper cells stimulate antibody responses to ABA which are qualitatively similar to those induced by GAT-specific helpers. However, ABA-specific helper cells do not permit the conversion of the I region gene-controlled nonresponder phenotype to GAT. The data suggests that high ABA density, which is required for optimal ABA help expression, extinguishes the immunogenicity of GAT determinants at both T and B cell levels.
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