CAJ | 학술논문

目的:本研究以Lewis肺癌细胞为研究对象,探讨肿瘤细胞通过TLRs对CD4~+ CD25~+ Treg细胞的影响.方法:我们采用流式细胞术检测了Lewis肺癌细胞与脾淋巴细胞共培养系统中CD4~+ CD25~+ Treg细胞数量变化;通过RT-PCR方法检测了共培养对Foxp3和TLR1-9mRNA表达的影响;采用TLR9受体阻断剂氯喹阻断Lewis肺癌TLR9的表达.结果:与对照组相比,共培养组CD4~+ CD25~+ Treg细胞数量及Foxp3 mRNA表达均明显增高(P＜0.05);Lewis肺癌细胞与淋巴细胞共培养后可影响多种TLRs表达,其中TLR9 mRNA表达与对照组相比明显增高(P＜0.05),阻断Lewis肺癌细胞TLR9可明显降低CD4~+ CD25~+ Treg细胞数量及Foxp3 mRNA表达(P＜0.05).结论:Lewis肺癌细胞可通过TLR9促进CD4~+ CD25~+ Treg细胞产生及功能增强,参与诱导肿瘤的免疫耐受,从而促进肿瘤的发生和发展.
목적:본연구이Lewis폐암세포위연구대상,탐토종류세포통과TLRs대CD4~+ CD25~+ Treg세포적영향.방법:아문채용류식세포술검측료Lewis폐암세포여비림파세포공배양계통중CD4~+ CD25~+ Treg세포수량변화;통과RT-PCR방법검측료공배양대Foxp3화TLR1-9mRNA표체적영향;채용TLR9수체조단제록규조단Lewis폐암TLR9적표체.결과:여대조조상비,공배양조CD4~+ CD25~+ Treg세포수량급Foxp3 mRNA표체균명현증고(P＜0.05);Lewis폐암세포여림파세포공배양후가영향다충TLRs표체,기중TLR9 mRNA표체여대조조상비명현증고(P＜0.05),조단Lewis폐암세포TLR9가명현강저CD4~+ CD25~+ Treg세포수량급Foxp3 mRNA표체(P＜0.05).결론:Lewis폐암세포가통과TLR9촉진CD4~+ CD25~+ Treg세포산생급공능증강,삼여유도종류적면역내수,종이촉진종류적발생화발전.
Objective:To explore the influence of tumor cells on CD4~+ CD25~+ Treg cells via TLRs.Methods:The numbers changes of CD4~+ CD25~+ Treg cells in the co-culture system of Lewis lung cancer cells and splenic lymphocytes were detected by flow cytometry;The expression of Foxp3 and TLR1-9 mRNA after co-culture were detected by RT-PCR;TLR9 expression on Lewis lung cancer cells was blocked by TLR9 receptor antagonist chloroquine.Results:Compared with control group,the number of CD4~+ CD25~+ Treg cells and Foxp3 mRNA expression were significantly increased in the co-culture group (P＜0.05).The expression of a variety of TLRs were affected by the co-culture of lymphocytes with Lewis lung cancer cells,and TLR9 mRNA expression was significantly increased compared with that of the control group (P＜0.05);Blocking TLR9 of Lewis lung cancer cells significantly reduce CD4~+ CD25~+ Treg cells and Foxp3 mRNA (P＜0.05).Conclusion:Lewis lung cancer cells could increase both number and function of CD4~+ CD25~+ Treg cells through inducing TLR9 expression in immunocells.This might be one of mechanisms of tumor-induced immune tolerance,and by which to contribute to the occurrence and progression of tumors.