Induction of a ragweed-specific allergic state in Ir-gene-restricted nonresponder mice.
Mice of the inbred strains, C57BL/6 and C57BL/10 (H-2b), are genetically incapable of developing IgE antibody responses to ragweed pollen extract (RE) or its dinitrophenylated derivative, DNP-RE. This nonresponsiveness has previously been thought to reflect the absence of a relevant H-2-linked Ir genes controlling responses of inbred mice to these antigens. However, pretreatment of H-2b mice with either low doses of ionizing X irradiation or cyclophosphamide abrogates the nonresponder status of such animals, apparently by removal of a suppressive mechanism normally inhibiting development of IgE responses to these antigens. The implications of these findings for mechanisms of genetic control of IgE antibody synthesis and the Ir-gene concept are discussed.
D000818:Animals; D000906:Antibodies / Q000032:analysis; D000921:Antibody-Producing Cells; D003520:Cyclophosphamide / Q000494:pharmacology; D004140:Dinitrophenols / Q000276:immunology; D005260:Female; D006649:Histocompatibility Antigens; D007073:Immunoglobulin E; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D011058:Pollen; D011830:Radiation Effects; D013489:Suppression, Genetic; D013601:T-Lymphocytes / Q000276:immunology
D000906:Antibodies; D004140:Dinitrophenols; D006649:Histocompatibility Antigens; D007073:Immunoglobulin E; D003520:Cyclophosphamide