Zimmerman M J, Radford-Smith G R, Jewell D P
Gastroenterology Department, Royal Perth Hospital, Western Australia, Australia.
Mediators Inflamm. 1998;7(1):7-11. doi: 10.1080/09629359891315.
The aim of this study was to assess whether interleukin-10 (IL-10) and/or transforming growth factor beta-1 (TGFbeta1) downregulate HLA-DR expression using the HT29 cell line as a model of colonic epithelial cells. HLA-DR expression was induced in HT29 cells with gamma-interferon. The effects of IL-10 alone, TGFbeta1 alone, and IL-10 and TGFbeta1 in combination were studied. HLA-DR expression was assessed using flow cytometric analysis. Gamma-interferon induced HLA-DR expression in a dose-dependent fashion. In the absence of gamma-interferon, neither IL-10 nor TGFbeta1 induced HLA-DR expression. In isolation, neither IL-10 nor TGFbeta1 downregulated HLA-DR expression. When IL-10 and TGFbeta1 were added in combination, small (6-30%) statistically significant reductions in HLA-DR expression were seen. The biological significance is unclear.
本研究的目的是使用HT29细胞系作为结肠上皮细胞模型,评估白细胞介素-10(IL-10)和/或转化生长因子β-1(TGFβ1)是否下调HLA-DR表达。用γ干扰素诱导HT29细胞中的HLA-DR表达。研究了单独的IL-10、单独的TGFβ1以及IL-10和TGFβ1联合使用的效果。使用流式细胞术分析评估HLA-DR表达。γ干扰素以剂量依赖性方式诱导HLA-DR表达。在没有γ干扰素的情况下,IL-10和TGFβ1均未诱导HLA-DR表达。单独使用时,IL-10和TGFβ1均未下调HLA-DR表达。当联合添加IL-10和TGFβ1时,观察到HLA-DR表达有小幅度(6%-30%)的统计学显著降低。其生物学意义尚不清楚。