Department of Orthopedics, Shenyang Military Region General Hospital, Shengyang, China.
Department of Orthopedics, Shenyang Orthopaedic Hospital, Shengyang, China.
J Int Med Res. 2020 Mar;48(3):300060519896892. doi: 10.1177/0300060519896892.
Vitamin D (VD) deficiency increases susceptibility to tuberculosis and is an important immunomodulator. Dendritic cells (DCs) are important antigen-presenting cells that play a critical role during tuberculosis infection, and modulates DC responses. The underlying mechanism is poorly understood. Our aim was to study changes in DC surface markers in VD deficient mice administered Bacillus Calmette-Guérin (BCG).
We divided C57BL/6 mice into a normal group and a VD deficient group. Two groups of mouse bone marrow-derived cells were isolated and cultured with granulocyte-macrophage colony-stimulating factor (20 ng/mL) and interleukin-4 (10 ng/mL) for 6 days. On day 7, BCG (0, 1 or 2 mg/mL) was administered to both groups for 24 hours. Non-adherent cells were harvested to assess DC phenotypic changes induced by different concentrations of BCG.
Expression levels of CD80, MHC-I, MHC-II and CD86 on the surfaces of DCs from VD deficient mice were lower than those in DCs from normal mice. By contrast, the expression level of CD11c on DCs was higher in VD deficient mice than in normal mice. Changes in all factors were concentration-dependent.
These findings indicate that BCG reduced DC surface marker expression to modulate immune responses during infection.
维生素 D（VD）缺乏会增加感染结核病的易感性，并且是一种重要的免疫调节剂。树突状细胞（DC）是重要的抗原呈递细胞，在结核病感染过程中发挥关键作用，并调节 DC 反应。其潜在机制尚不清楚。我们的目的是研究在给予卡介苗（BCG）的维生素 D 缺乏小鼠中 DC 表面标志物的变化。
我们将 C57BL/6 小鼠分为正常组和 VD 缺乏组。两组小鼠的骨髓细胞均分离并在粒细胞巨噬细胞集落刺激因子（20ng/mL）和白细胞介素-4（10ng/mL）的作用下培养 6 天。第 7 天，用不同浓度的 BCG（0、1 或 2mg/mL）处理两组 24 小时。收获非粘附细胞，以评估不同浓度 BCG 诱导的 DC 表型变化。
VD 缺乏小鼠 DC 表面的 CD80、MHC-I、MHC-II 和 CD86 表达水平低于正常小鼠 DC。相比之下，VD 缺乏小鼠的 DC 表面 CD11c 表达水平高于正常小鼠。所有因素的变化均呈浓度依赖性。
这些发现表明 BCG 通过降低 DC 表面标志物的表达来调节感染期间的免疫反应。
