Selenium deficiency inhibits differentiation and immune function and imbalances the Th1/Th2 of dendritic cells

Abstract

Selenium (Se) deficiency inhibits immune cell differentiation, affects immune response, and leads to cellular and humoral immune dysfunction. However, the impact of Se deficiency on the differentiation and Th1/Th2 balance of dendritic cells is still unclear. In this study, we replicated a model of Se-deficient chickens by feeding the chickens with a low-Se diet (i.e., the content of Se is 0.008 mg per kg diet). On this basis, we explored the effect of Se deficiency on the differentiation of chicken dendritic cells by induction culture of peripheral blood monocyte cells. We induced chicken dendritic cells by incubating mononuclear cells with a 100 ng mL⁻¹ recombinant chicken granulocyte-macrophage colony-stimulating factor and 20 ng mL⁻¹ recombinant chicken IL-4 for total 7 days. The results showed that Se deficiency decreased the expression of cell-surface markers including CD11c, CD40, CD86, and MHC II. Furthermore, we analyzed the cytokine profiles using real-time quantitative PCR and ELISA. The results indicated that Se deficiency inhibited the expression of selenoproteins and changed the secretion of IL-10, IL-12p40, and IFN-γ. Additionally, Se deficiency weakened the ability of dendritic cells to stimulate the proliferation of mixed allogeneic lymphocytes. In conclusion, Se deficiency suppressed the differentiation and immune function of chicken dendritic cells by down-regulating the expression of CD11c, CD40, CD86, MHC II, and selenoproteins. The result also showed that the Th1/Th2 imbalance was induced by enhancing the secretion of Th1-type cytokine IL-12p40 and IFN-γ and reducing that of Th2-type cytokine IL-10. Our findings contribute to understanding the mechanism of Se deficiency in the differentiation and immune function of chicken dendritic cells.