CAJ | 학술논문

本研究探讨干扰素α(IFN-α)对慢性髓系白血病(CML)来源树突状细胞(DC)表达趋化因子CCR7及分泌IL-10、IL-12 P70的影响.在诱导CML-DCs的无血清条件培养基中,除加入SCT、GM-CSF、TNF-α及IL-4外,还加入不同浓度IFN-α.培养10-14天后,用流式细胞术检测共刺激分子及CCR7表达,G显带法显示Ph1染色体,噻唑蓝(MTT)法检测CML-DC刺激正常人外周血淋巴细胞增殖状况,ELISA法检测培养上清IL-10及IL-12P70含量.结果显示:IFN-α(300 U/ml)组与无IFN-α组比较其CML-Dc的CD40、CD83、CD86及CCR7的表达均升高1倍,异体混合淋巴细胞反应(MLR)中OD值增加1倍,Phl染色体阳性比例及IL-10和IL-12 P70浓度均减低.结论:IFN-α能够部分纠正CML-DC免疫表型及功能缺陷,这同其上调DC共刺激分子和CCR7表达及解除了CML血清中IL-10对CML-DC分化的抑制有关.
본연구탐토간우소α(IFN-α)대만성수계백혈병(CML)래원수돌상세포(DC)표체추화인자CCR7급분비IL-10、IL-12 P70적영향.재유도CML-DCs적무혈청조건배양기중,제가입SCT、GM-CSF、TNF-α급IL-4외,환가입불동농도IFN-α.배양10-14천후,용류식세포술검측공자격분자급CCR7표체,G현대법현시Ph1염색체,새서람(MTT)법검측CML-DC자격정상인외주혈림파세포증식상황,ELISA법검측배양상청IL-10급IL-12P70함량.결과현시:IFN-α(300 U/ml)조여무IFN-α조비교기CML-Dc적CD40、CD83、CD86급CCR7적표체균승고1배,이체혼합림파세포반응(MLR)중OD치증가1배,Phl염색체양성비례급IL-10화IL-12 P70농도균감저.결론:IFN-α능구부분규정CML-DC면역표형급공능결함,저동기상조DC공자격분자화CCR7표체급해제료CML혈청중IL-10대CML-DC분화적억제유관.
This study was aimed to investigate the influences of interferonα(IFN-α)on expressions of CCR7,interleukin10(IL-10)and IL-12p70 in dendritic cells(DCs)from patients with chronic myeloid leukcmia(CML).In addition to stem cell factor(SCF),granulocytc-macrophage colony stimulating factor(GM-CSF),tumor necrosis factor-α (INF-α)and IL-4,IFN-α was added to the serum-free medium of DCs.After culture for 10-14 days,phenotypes and function of CML-DCs were evaluated respectively by flow cytometry and methyl thiazolyl tetrazolium(MTT)assay.Chromosome of DCs was analyzed by displaying G banding assay.The concentrations of IL-10 and IL-12P70 in supernarants were evaluated by enzyme-linked immunosorbent assay(EUSA).The results showed that the expressions of CD40,CD83,CD86 and CCR7 and the OD value in allogeneic mixed-lymphocyte reaction(MLR)in group with IFN-α (300 U/ml) were twice as high as those in group without IFN-α.The percentage of Ph1 positive cells and concentrations of IL-10 and IL-12 P70 were reduced in group with IFN-α.It is concluded that the defective phenotypes and functions of CML-DCs can be recruited partly by IFN-α.The mechanism may lie in the facts that expression of CCR7 and co-stimulatory molecules is promoted and the inhibitory effect of IL-10 on CML-DCs is relieved partly through the regulation of IFN-α.