Department of Clinical Laboratory, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, Jiangsu Province, People's Republic of China.
Inflammation. 2015;38(3):1322-8. doi: 10.1007/s10753-014-0103-z.
This study aimed to investigate molecule B7-H3 expression profiles of patients with ankylosing spondylitis (AS) and the clinical significance of B7-H3 in the pathogenesis of AS. Serum B7-H3 levels were measured by ELISA in patients with AS and healthy controls. The expression of B7-H3 protein and mRNA on CD14+ monocytes of peripheral blood mononuclear cells (PBMCs) and serum levels of T cell-associated cytokines were also analyzed. The serum B7-H3 levels in AS patients were significantly lower than in healthy controls. The expression of B7-H3 protein and mRNA on CD14+ monocytes of PBMCs and serum levels of TNF-α, IL-6, and IL-17A in AS patients were significantly higher than in controls. The reduced serum B7-H3 level was highly negatively correlated with AS Disease Activity Score (ASDAS), TNF-α, and IL-17A. Upregulated B7-H3 protein may play a role in the pathogenesis of AS by binding its receptor on T cells.
本研究旨在探讨强直性脊柱炎(AS)患者 B7-H3 分子表达谱及 B7-H3 在 AS 发病机制中的临床意义。采用 ELISA 法检测 AS 患者和健康对照者血清 B7-H3 水平,分析外周血单个核细胞(PBMCs)CD14+单核细胞上 B7-H3 蛋白和 mRNA 的表达及 T 细胞相关细胞因子的血清水平。AS 患者血清 B7-H3 水平明显低于健康对照组,AS 患者 PBMCsCD14+单核细胞上 B7-H3 蛋白和 mRNA 的表达及 TNF-α、IL-6、IL-17A 血清水平明显高于对照组。血清 B7-H3 水平降低与 AS 疾病活动评分(ASDAS)、TNF-α 和 IL-17A 呈高度负相关。上调的 B7-H3 蛋白可能通过与其在 T 细胞上的受体结合在 AS 的发病机制中发挥作用。