Major reproduction hormones as regulators of cell-to-cell interactions in humoral immune responses.

The effects of chorionic gonadotropin (CG), estradiol, and progesterone on the cell mechanisms that determine the rate of the humoral immune response have been investigated in experiments on ovariectomized and noncastrated mice. CG (40 IU) injected into noncastrated animals increased the antibody response to sheep erythrocytes (SRBC), whereas a higher dose of the hormone (200 IU) had no effect. In contrast, both hormone doses inhibited the immune response in ovariectomized animals. Injection of estradiol (2.5 micrograms/day), but not progesterone (0.2 mg/day), into ovariectomized mice stimulated the immune response, indicating a possible role of estrogens as mediators of CG immuno-stimulating effect in noncastrated animals. Both CG does inhibited suppressor cell generation in noncastrated mice, whereas in ovariectomized animals, the hormonal effect was directly opposite. Sex steroid hormones did not influence the formation of suppressor cells. In a syngeneic transfer system, the hormones under study did not change the activity of helper T cell precursors. However, CG administration to noncastrated recipients stimulated an adoptive immune response in a dose-dependent manner. Estradiol, but not progesterone, has the same effect in ovariectomized mice. CG administration (200 IU) to ovariectomized recipients inhibited the plaque-forming cell response. This CG effect depended upon prostaglandin synthetase activity.