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Suppression of the immune response to altered self induced by immunogenic and nonimmunogenic altered self structures
Fluorescein (FITC)-haptenated mouse spleen cells are capable of inducing a B cell immune response characterized by the production of antibodies directed against hapten-altered self structures. The induction of this response is thymus-independent and strictly dependent on the hapten concentration used for labeling the cells. Pretreatment of mice with immunogenic, labeled spleen cells strongly suppressed the plaque-forming cell response to a subsequent challenge with FITC-labeled spleen cells, sheep (SRC) or horse (HRC) red cells labeled with the same hapten and native FITC-dextran. Mice primed with lightly haptenated (nonimmunogenic) cells 7 days before challenge were completely unresponsive to the immunogenic dose of labeled cells and displayed a significantly reduced response to FITC-SRC or FITC-HRC. However, the response to FITC-dextran was enhanced, as compared to unprimed animals. The concept of immunogenic vs. nonimmunogenic requirements of an antigen to induce unresponsiveness, and the specificity of the B cell clones affected by suppression is discussed.
Fluorescein (FITC)-haptenated mouse spleen cells are capable of inducing a B cell immune response characterized by the production of antibodies directed against hapten-altered self structures. The induction of this response is thymus-independent and strictly dependent on the hapten concentration used for labeling the cells. Pretreatment of mice with immunogenic, labeled spleen cells strongly suppressed the plaque-forming cell response to a subsequent challenge with FITC-labeled spleen cells, sheep (SRC) or horse (HRC) red cells labeled with the same hapten and native FITC-dextran. Mice primed with lightly haptenated (nonimmunogenic) cells 7 days before challenge were completely unresponsive to the immunogenic dose of labeled cells and displayed a significantly reduced response to FITC-SRC or FITC-HRC. However, the response to FITC-dextran was enhanced, as compared to unprimed animals. The concept of immunogenic vs. nonimmunogenic requirements of an antigen to induce unresponsiveness, and the specificity of the B cell clones affected by suppression is discussed.