Prolactin modulates the functions of murine spleen CD11c-positive dendritic cells.

Prolactin (PRL), an anterior pituitary polypeptide hormone, has been shown to have a role in the immunomodulation. Some reports have shown the importance of PRL in activating lymphocytes and macrophages. To further investigate the effect of PRL on the immune system in vitro, murine spleen CD11c-positive dendritic cells (SDCs) were treated with various concentrations of PRL for 24 h, then their viability, phenotype, nuclear factor kappa B p65 (NF-kappaBp65), endocytosis, stimulatory capacity, and cytokine expression were analyzed. The results showed that PRL increased the viability and stimulatory capacity of SDCs, up-regulated the expressions of MHC-11 and CD40 while decreased the level of CD54 on SDCs. Furthermore, PRL decreased the level of NF-kappaBp65 and the endocytosis of SDCs. In addition, PRL increased the expressions of IL-6, IL-10, IL-12 and TNF-alpha in SDCs. These data suggested that PRL might regulate the physiological and pathological immune responses by changing the viability, phenotype, NF-kappaBp65, endocytosis, stimulatory capacity, and cytokine expression of SDCs.