Estradiol regulation of thymic lymphocyte function in the rat: mediation by serum thymic factors.

Estradiol (E2) can depress the function of the thymic lymphocytes. To determine if this response to a gonadal steroid is regulated directly or indirectly, thymic lymphocytes were incubated in vitro for 3 days in the presence of the mitogens concanavalin A (Con A) or phytohaemagglutinin (PHA) + tissue culture media + 20% specific rat serum fractions and pulse labelled with tritiated thymidine. Rat serum fractions were prepared from control, castrate, thymectomized (Tx) and castrate-Tx animals as well as from similar groups of animals treated in vivo for three days with physiological doses of E2. It was found that there was a significant enhancement of thymocyte blastogenesis in cultures incubated with castrate rat serum + Con A or PHA vs. control serum cultures (P less than 0.001). Direct replacement of E2 to castrate sera in vitro at physiological concentrations failed to depress thymocyte blastogenesis to noncastrate levels. Sera prepared from castrate animals treated with E2 at physiological concentrations was successful in depressing the blastogenic response to noncastrate levels. Sera from Tx animals did not enhance Con A induced blastogenesis, but PHA response was significantly increased (P less than 0.01) This effect was lost utilizing sera from Tx animals treated with E2. It is concluded that thymocyte function is regulated by serum factors which have their origin in the thymus, and that these factors are modulated by a gonadal steroid estradiol.