本文選題：關(guān)節(jié)炎 + 類風(fēng)濕　； 參考：《北京大學(xué)學(xué)報(bào)(醫(yī)學(xué)版)》2016年06期

【摘要】：目的:明確半乳糖凝集素1(galectin-1)在臍帶間充質(zhì)干細(xì)胞(umbilical cord mesenchymal stem cells,UCMSCs)調(diào)控類風(fēng)濕關(guān)節(jié)炎(rheumatoid arthritis,RA)患者T細(xì)胞功能中的作用。方法:應(yīng)用慢病毒構(gòu)建galectin-1低表達(dá)的UC-MSCs,即UC-MSCs(Gal-1-),采用直接接觸培養(yǎng)方式分別將UC-MSCs、UC-MSCs(Gal-1-)與RA患者的CD4~+T細(xì)胞共培養(yǎng)。設(shè)立陰性對照組(CD4~+T)、陽性對照組[CD4~+T培養(yǎng)過程中加入植物血凝素(phytohaemagg lutinin,PHA)2 mg/L]、UC-MSCs-CD4~+T共培養(yǎng)組、UC-MSCs(對照shRNA)-CD4~+T共培養(yǎng)組及UC-MSCs(Gal-1-)-CD4~+T共培養(yǎng)組。MTS法檢測CD4~+T細(xì)胞增殖,ELISA方法檢測共培養(yǎng)上清液中腫瘤壞死因子α(tumor necrosis factorsα,TNF-α)水平,流式細(xì)胞術(shù)檢測Th1/Th2/Th17細(xì)胞亞型。結(jié)果:UC-MSCs和UC-MSCs(對照shRNA)與CD4~+T細(xì)胞共培養(yǎng)組可顯著抑制PHA誘導(dǎo)的CD4~+T細(xì)胞增殖及TNF-α表達(dá),而UC-MSCs(Gal-1-)組對此無明顯抑制作用。與陰性對照組(8.51%±2.04%)相比,UC-MSCs及UC-MSCs(對照shRNA)組可顯著抑制Th1細(xì)胞分化(分別為4.83%±1.37%和5.13%±0.87%,P值分別為0.012和0.018),而UC-MSCs(Gal-1-)組對此無明顯抑制作用(6.41%±0.96%,P=0.101)。與陰性對照組相比,UC-MSCs及UC-MSCs(對照shRNA)組可上調(diào)Th2并下調(diào)Th17比例,但差異并無統(tǒng)計(jì)學(xué)意義,UC-MSCs(Gal-1-)組的這一作用不明顯。結(jié)論:UC-MSCs可抑制RA患者CD4~+T細(xì)胞的增殖、活化并可降低Th1細(xì)胞比例,但敲低galectin-1分子的表達(dá)后該作用減弱,提示galectin-1參與了UC-MSCs抑制RA患者CD4~+T細(xì)胞功能的過程。
[Abstract]:Aim: to investigate the role of galactose-1galectin-1 in the regulation of T cell function in patients with rheumatoid arthritis (RA) by umbilical cord mesenchymal cord mesenchymal stem cells (UCMSCs).Methods: Lentivirus was used to construct the low expression UC-MSCs (UC-MSCs), or UC-MSCs Gal-1-T cells. The UC-MSCsSU UC-MSCs Gal-1 was co-cultured with the CD4T cells of RA patients by direct contact culture.A negative control group was established, and the positive control group [phytohaemagglutinin lutinin PHA2 mg/L] UC-MSCs-CD4T co-culture group (control shRNA-CD4T co-culture group and UC-MSCsGal-1-CD4T co-culture group. MTS method was used to detect the proliferation of CD4T cells by Elisa.The level of tumor necrosis factor 偽 necrosis factors 偽 (TNF- 偽) in supernatant,The subtypes of Th1/Th2/Th17 cells were detected by flow cytometry.Results the PHA induced proliferation of CD4T cells and the expression of TNF- 偽 were significantly inhibited in the two groups, but not in the UC-MSCs and UC-MSCsGal-1-treated groups, but not in the UC-MSCs and UC-MSCs co-cultured with CD4T cells, but the expression of TNF- 偽 was not significantly inhibited in the UC-MSCs and UC-MSCs Gal-1-treated groups.Compared with the negative control group (8.51% 鹵2.04%), UC-MSCs and UC-MSCs significantly inhibited the differentiation of Th1 cells (4.83% 鹵1.37% and 5.13% 鹵0.87%, P = 0.012 and 0.018%, respectively).Compared with negative control group, UC-MSCs and UC-MSCs could up-regulate Th2 and down-regulate the proportion of Th17, but the difference was not significant in UC-MSCs Gal-1-treated group.Conclusion: WUC-MSCs can inhibit the proliferation of CD4T cells, activate the CD4T cells and decrease the proportion of Th1 cells in RA patients, but the expression of galectin-1 molecules is weakened after knockdown, suggesting that galectin-1 plays an important role in the inhibition of CD4T cell function in RA patients by UC-MSCs.
【作者單位】： 北京大學(xué)第三醫(yī)院風(fēng)濕免疫科;
【基金】：國家自然科學(xué)基金(81273293)資助~~
【分類號】：R593.22

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