Effects of 17beta-estradiol on the maturation, nuclear factor kappa B p65 and functions of murine spleen CD11c-positive dendritic cells.

Physiological gender differences in immune capabilities are now well recognized and suggest that sex steroid hormones such as estrogens may be involved in the regulation of the immunocompetence. In this paper, CD11c-positive murine spleen dendritic cells (SDCs) were treated with various concentrations of 17beta-estradiol (E2) for 24h. The viability, phenotype, nuclear factor kappa B p65 (NF-kappaBp65), endocytosis, stimulatory capacity and cytokine expression were analyzed. Our results showed that E2 increased the viability and MHC-II expression but decreased nuclear NF-kappaBp65 level and endocytosis of SDCs. E2 also increased the stimulatory capacity of SDCs from low-dose group but decreased it from middle- and high-dose ones. In addition, E2 increased the intracellular expression of IL-6 and IL-10 in SDCs, but no obvious change appeared in IL-12 and TNF-alpha. These data suggested that E2 might influence the immune responses by changing the viability, maturation, NF-kappaBp65, endocytosis, stimulatory capacity and cytokine expression of SDCs.