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Updated: Aug 10, 2026

Overcoming Unresponsiveness in Experimental Autoimmune Encephalomyelitis (EAE) Resistant Mouse Strains by Adoptive Transfer and Antigenic Challenge
Published on: April 9, 2012
IgE antibody-specific abrogation of an established immune response in mice by modified antigens
DBA/1 mice were immunized with low doses of ovalbumin and alumina gel to elicit an IgE response which could be augmented upon reimmunization. Treatment of IgE-producing mice with high doses of chemically modified ovalbumin preparations markedly reduced or eliminated the ability of the mice to respond to subsequent reimmunizations with low doses of ovalbumin. It was found that the primary structural requirement for efficacy of the modified ovalbumins was reduced antigenicity to prevent the anaphylactic demise of the animals. Cumulative doses of 0.5 mg or more given in several increments, i.v., afforded optimal protection. The protection was antigen-specific and persisted for 2 to 3 months regardless of intervening exposures of the animals to low doses of antigen. It could be extended by further courses of treatment. There was no correlation between the levels of circulating hemagglutinating or total antibody and the induction of unresponsiveness. Nor was the passive administration of antibody able to approximate the effects of the modified antigens. It is suggested that the induction of the IgE class specific unresponsiveness in responding animals may take p;ace via effects on T cells.
DBA/1 mice were immunized with low doses of ovalbumin and alumina gel to elicit an IgE response which could be augmented upon reimmunization. Treatment of IgE-producing mice with high doses of chemically modified ovalbumin preparations markedly reduced or eliminated the ability of the mice to respond to subsequent reimmunizations with low doses of ovalbumin. It was found that the primary structural requirement for efficacy of the modified ovalbumins was reduced antigenicity to prevent the anaphylactic demise of the animals. Cumulative doses of 0.5 mg or more given in several increments, i.v., afforded optimal protection. The protection was antigen-specific and persisted for 2 to 3 months regardless of intervening exposures of the animals to low doses of antigen. It could be extended by further courses of treatment. There was no correlation between the levels of circulating hemagglutinating or total antibody and the induction of unresponsiveness. Nor was the passive administration of antibody able to approximate the effects of the modified antigens. It is suggested that the induction of the IgE class specific unresponsiveness in responding animals may take p;ace via effects on T cells.
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