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机构地区:[1]山西省人民医院普外科,太原030012 [2]山西医科大学第一附属医院普外科 [3]华中科技大学同济医学院附属协和医院胰腺外科
出 处:《中华实验外科杂志》2009年第7期852-854,共3页Chinese Journal of Experimental Surgery
基 金:2009年山西省自然科学基金资助项目(2009011052-2)
摘 要:目的观察胰腺癌微环境对树突状细胞(DC)成熟的影响及功能变化并探讨胰腺肿瘤细胞免疫逃逸的机制。方法培养树突状细胞,加入粒细胞巨噬细胞集落刺激因子(rmGM-CSV)40μg/L、白细胞介素(IL)-440μg/L,培养到第6天时得到大量的未成熟树突状细胞(imDC),加入大鼠胰腺癌细胞(AR42J cell)培养上清液诱导,流式细胞术检测DC的表面分子CD86、CD80的表达(n=6),观察能否延缓或阻断imDC的成熟及其在脂多糖(LPS)刺激后这种作用能否被逆转。并观察AR42J细胞培养上清诱导的DC对同种异体混合淋巴细胞增殖。结果加入胰腺癌癌细胞上清液培养的DC,与正常成熟的DC比较,CD80^+CD86^+阳性率由(70.88±3.60)%降至(7.15±0.71)%,LPS刺激后DC细胞的表面分子CD80^+CD86^+表达仍然较低(7.43±1.05)%,表明胰腺癌细胞培养上清液对DC的成熟有阻断作用。AR42J细胞上清诱导培养的imDC组刺激同种异体混合淋巴细胞增殖的强度显著低于正常培养的imDC组刺激同种异体混合淋巴细胞增殖的强度。结论体外大鼠胰腺癌细胞培养上清液可以诱导DC处于不成熟状态,且这种不成熟状态不容易被逆转。Objective To study the effect of pancreatic cancer microenvironment on maturation of dendritic cells ( DCs), and to investigate the mechanism by which tumors escape from immune recognition. Methods DCs were cultured with rmGM (40 μg/L) ,rmIL-4 (40 μg/L) ,and the supernatant of cell line AR42J cells was added on the day 6, then a large number of DCs was gained. DCs cultured and induced by routine methods were used as controls. The expression of surface molecules CD86, and CD80 in DCs was detected to observe whether this intervention could delay or block maturation of DCs and this effect could be reversed by stimulation with lipopolysaccharide (LPS). T cell stimulatory effects were also determined. Results Compared to normal DCs,CD86 and CD80 expression positive rate was significantly decreased in DCs induced by AR42J supematant from (70.88 ± 3.60)% to (7.15 ± 0.71 )%. After stimulation with LPS, the expression of CD86, and CD80 in DCs was still low, suggesting the AR42J supernatant could block the maturation of DCs. The allostimulatory capacity of the immature DCs stimulated with the AR42J supematant was significantly lower than that of the normal immature DCs. Conclusion The supematant from pancreatic cancer cells in rats could inhibit the maturation of DCs, which was not easily reversed.
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