Vitamin D has been reported to regulate the maturation and function of dendritic cells (DCs). Obesity was shown to be associated with the dysregulation of vitamin D metabolism and malfunction of DCs. We investigated the effects of in vitro 1,25(OH)₂D₃ treatment (0, 1, or 10 nM) on phenotype and expression of genes related to function of bone marrow-derived DCs (BMDCs) from control and obese mice. C57BL/6 N mice were fed a control or high-fat (10% or 45% kcal fat: CON or HFD) diets for 15 weeks. Differentiation toward DCs was induced with GM-CSF (20 ng/ml) and maturation was induced by LPS (50 ng/ml); 10 nM 1,25(OH)₂D₃ treatment inhibited BMDC differentiation (CD11c⁺) and decreased the percentage of mature DCs (MHCII^highCD11c⁺ and CD86^highCD11c⁺) in both CON and HFD groups. The Il10 expression in stimulated BMDCs from the CON group increased with the 10 nM 1,25(OH)₂D₃ treatment, but not in those from the HFD group. The Il12b mRNA levels in stimulated BMDCs were lower in the HFD group than in the CON group. In conclusion, lower levels of Cd 40, Cd83 and Il12 mRNA in LPS-stimulated BMDCs from obese mice suggest malfunction of DCs as antigen presenting cells. 1,25(OH)₂D₃ treatment inhibited the differentiation and maturation of BMDCs in both control and obese mice. Differential effects of 1,25(OH)₂D₃ on the expression of Il10 between control and obese mice suggest that regulation of immune response by vitamin D could be influenced by obesity.

据报道维生素D调节树突状细胞（DCs）的成熟和功能。肥胖被证明与维生素D代谢失调和DC功能障碍有关。我们调查了体外1,25（OH）₂ D ₃处理（0、1或10 nM）对表型和基因表达的影响，这些基因与来自对照和肥胖小鼠的骨髓DCs（BMDCs）的功能有关。给C57BL / 6 N小鼠喂食对照或高脂（10％或45％大卡脂肪：CON或HFD）饮食15周。GM-CSF（20 ng / ml）诱导向DC分化，LPS（50 ng / ml）诱导成熟。10 nM 1,25（OH）₂ D ₃处理抑制BMDC分化（CD11c ⁺），降低了CON和HFD组中成熟DC的百分比（MHCII^高CD11c ⁺和CD86^高CD11c ⁺）。所述IL10从CON组在受刺激的BMDC表达与10nM的1,25（OH）增加₂ d ₃治疗，但不是在那些从HFD组。HFD组受刺激的BMDC中的Il12b mRNA水平低于CON组。总之，来自肥胖小鼠的LPS刺激的BMDC中Cd 40，Cd83和Il12 mRNA的较低水平表明DC作为抗原呈递细胞的功能障碍。1,25（羟基）₂ D ₃在对照组和肥胖小鼠中，这种治疗均抑制了BMDC的分化和成熟。1,25（OH）₂ D ₃对对照小鼠和肥胖小鼠中IL10表达的不同影响表明，肥胖可能影响维生素D对免疫应答的调节。