Sex hormones and the immune response. II. Perturbation of antibody production by estradiol 17beta.

The administration of 75 microgram/kg of estradiol 17beta at successively later stages in the immune response of female guinea pigs to penicilloyl-coupled cavian globulins showed that this steroid reduces the rate of attainment of the maximum titer, the magnitude of the titer achieved, and the rate of titer decay. Control titers maximized at the third experimental week and diminished to one third the peak value by the 6th week. When steroid treatment was begun coincidentally with inoculation (week 0), the peak titer was delayed by 3 weeks, and by 2 weeks when hormone priming was begun at week 1 or 2. The highest antibody titers achieved in the presence of estrogen were 25-30% lower than those of sesame oil controls. The greatest immunosuppressive effect was observed when estradiol was given at the peak of the immune response, the titer dropping by 50% and remaining at that level for the next 4 weeks in spite of continued antigen inoculation and steroid treatment. Titer decay after the end of the inoculation course was prevented by estradiol but not by progesterone, CHP, or these same oil vehicle.