Effect of interleukin-10 on the phenotype and function of cultured human dendritic cells

Dendritic cells (DCs) are potent antigen presenting cells (APCs), and are able to induce tissue like kidney immune-inflammatory responses. 1,2 DCs can either stimulate immune responses or induce immune tolerance, according to its mature states.1 DCs undergo a series of maturational steps that allow them to up-regulate surface adhesion molecules and co-stimulation molecules, as well as increase secretion of interleukin (IL)-12, all of which have the pivotal effects on DC functions.1 Several cytokines are known to contribute to this process. Renal diseases are immune-inflammatory diseases. In their immunopathological injury processes, many cytokines in the network of mutual promotion or antagonism modulate the balance of Th1/Th2 immune responses that alter the development of diseases. Previous studies showed that IL-12 produced by DCs and monocyte/phagocyte in the inflammatory tissues could induce the differentiation of Th0 cells to Th1 cells, thus involved in renal immune-inflammatory development and injury. 3,4 It is known that IL-10 is a negative regulator in the immunopathological injury, which plays an important role in suppressing Th1 cellular immunity.5 In view of our previous study, it was demonstrated that many DCs distributed in the hepatic and renal tissues during the hepatic/renal ischemia-reperfusion injury.6 Therefore, in this study, we further investigated effect of IL-10 on DC phenotype and the secretion of IL-12 in vitro , providing an experimental basis for therapeutic intervention in immune-inflammatory diseases.