Exposure of mice to low doses of ionizing x-irradiation at or near the time of primary immunization with 2,4-dinitrophenyl (DNP)-Ascaris suum extract (ASC) results in substantial enhancement of IgE anti-DNP antibody responses; the IgG antibody responses of such mice do not increase after such manipulations. This selective enhancement of IgE antibody production occurs in mice of both high and low IgE responder phenotype, although the extent of enhancement compared to unmanipulated control animals is more striking in low IgE responder mice. The studies presented here demonstrate that the irradiation-enhanced IgE antibody responses of low responder SJL and C57BL/6 mice as well as of intermediate responder AKR mice can be effectively suppressed by passive transfer of CFA-immune serum obtained from isologous donor mice. Moreover, adoptive secondary IgE antibody responses in SJL recipients of primed syngeneic spleen cells can be totally abolished by passive transfer of CFA-immune serum or ascitic fluid from CFA-immune mice. The suppressive activity of CFA-immune serum can be diminished or eliminated by exposure of CFA-primed donor mice to low dose x-irradiation at an appropriate point during the priming regimen, after a single inoculation of CFA, and before collection of serum. Low dose x-irradiation was not effective in eliminating suppressive activity of CFA-induced ascites fluid obtained from donor mice inoculated repeatedly with CFA.
In contrast to the capacity of CFA-immune serum from isologous donors to suppress irradiation-enhanced IgE responses of low responder mice, similar sera or ascites fluids were ineffective in suppressing irradiation-enhanced responses of high responder BALB/c or (SJL × BALB/c)F1 hybrid mice. This was true irrespective of whether such sera or ascites were obtained from isologous donors or from donor mice of the low IgE responder phenotype. The implications of these findings with respect to clarifying some of the previously confusing observations concerning 1) the effects of adjuvant administration on IgE antibody production, and 2) differences in the capacities of different mouse strains to produce IgE antibodies in high vs low quantities are discussed.
This is publication No. 56 from the Department of Cellular and Developmental Immunology, and publication No. 1470 from the Immunology Departments, Scripps Clinic and Research Foundation, La Jolla, California. This work was supported by United States Public Health Service Grant AI-13874.