中华临床医师杂志（电子版）
中華臨床醫師雜誌（電子版）
중화림상의사잡지（전자판）
CHINESE JOURNAL OF CLINICIANS(ELECTRONIC VERSION)
2015年
12期
2355-2359
,共5页
DC细胞%LILRB2%干扰RNA%CD11c%CD80%CD86
DC細胞%LILRB2%榦擾RNA%CD11c%CD80%CD86
DC세포%LILRB2%간우RNA%CD11c%CD80%CD86
Dendritic cells%LILRB2%siRNA%CD11c%CD80%CD86
目的：探讨小鼠树突状细胞（DC）表面白细胞免疫球蛋白样受体2（LILRB2）改变对DC的CD11c、CD80和CD86表型的影响及意义。方法应用20 ng/ml重组小鼠粒细胞集落刺激因子（rGM-CSF）＋20 ng/ml IL-4刺激小鼠骨髓细胞生长，隔日进行细胞换液，第5天实验组转染LILRB2受体干扰RNA，空白对照组转染空质粒，对照组单纯换液。培养过程中观察细胞形态学变化，并于转染72 h后，光镜下观察DC形态，用流式细胞仪测定细胞表面CD11c、CD80和CD86分子表达。结果光镜下对照组与实验组均可见 DC 细胞形态，流式细胞仪测定实验组 CD11c （0.662±0.174）（n=12）与空白对照组 CD11c（0.675±0.237）和对照组（0.688±0.076）分子表达无明显差异（P＞0.05）。实验组 DC 细胞表面 CD80（0.626±0.060）较空白对照组 CD80（0.406±0.163）（n=12）和对照组CD80（0.409±0.100）表达均增加（P＜0.05）。实验组DC细胞表面CD86（0.730±0.102）较空白对照组CD86（0.497±0.278）和对照组CD86（0.368±0.073）表达均增加（P＜0.05）。结论应用LILRB2受体干扰RNA不影响DC细胞表面CD11c分子表达，而增加细胞表面CD80和CD86分子表达。细胞表面CD80和CD86分子作为免疫反应的重要协同刺激分子在抗原提呈细胞表面表达升高，则激活T细胞免疫反应的能力增强。
目的：探討小鼠樹突狀細胞（DC）錶麵白細胞免疫毬蛋白樣受體2（LILRB2）改變對DC的CD11c、CD80和CD86錶型的影響及意義。方法應用20 ng/ml重組小鼠粒細胞集落刺激因子（rGM-CSF）＋20 ng/ml IL-4刺激小鼠骨髓細胞生長，隔日進行細胞換液，第5天實驗組轉染LILRB2受體榦擾RNA，空白對照組轉染空質粒，對照組單純換液。培養過程中觀察細胞形態學變化，併于轉染72 h後，光鏡下觀察DC形態，用流式細胞儀測定細胞錶麵CD11c、CD80和CD86分子錶達。結果光鏡下對照組與實驗組均可見 DC 細胞形態，流式細胞儀測定實驗組 CD11c （0.662±0.174）（n=12）與空白對照組 CD11c（0.675±0.237）和對照組（0.688±0.076）分子錶達無明顯差異（P＞0.05）。實驗組 DC 細胞錶麵 CD80（0.626±0.060）較空白對照組 CD80（0.406±0.163）（n=12）和對照組CD80（0.409±0.100）錶達均增加（P＜0.05）。實驗組DC細胞錶麵CD86（0.730±0.102）較空白對照組CD86（0.497±0.278）和對照組CD86（0.368±0.073）錶達均增加（P＜0.05）。結論應用LILRB2受體榦擾RNA不影響DC細胞錶麵CD11c分子錶達，而增加細胞錶麵CD80和CD86分子錶達。細胞錶麵CD80和CD86分子作為免疫反應的重要協同刺激分子在抗原提呈細胞錶麵錶達升高，則激活T細胞免疫反應的能力增彊。
목적：탐토소서수돌상세포（DC）표면백세포면역구단백양수체2（LILRB2）개변대DC적CD11c、CD80화CD86표형적영향급의의。방법응용20 ng/ml중조소서립세포집락자격인자（rGM-CSF）＋20 ng/ml IL-4자격소서골수세포생장，격일진행세포환액，제5천실험조전염LILRB2수체간우RNA，공백대조조전염공질립，대조조단순환액。배양과정중관찰세포형태학변화，병우전염72 h후，광경하관찰DC형태，용류식세포의측정세포표면CD11c、CD80화CD86분자표체。결과광경하대조조여실험조균가견 DC 세포형태，류식세포의측정실험조 CD11c （0.662±0.174）（n=12）여공백대조조 CD11c（0.675±0.237）화대조조（0.688±0.076）분자표체무명현차이（P＞0.05）。실험조 DC 세포표면 CD80（0.626±0.060）교공백대조조 CD80（0.406±0.163）（n=12）화대조조CD80（0.409±0.100）표체균증가（P＜0.05）。실험조DC세포표면CD86（0.730±0.102）교공백대조조CD86（0.497±0.278）화대조조CD86（0.368±0.073）표체균증가（P＜0.05）。결론응용LILRB2수체간우RNA불영향DC세포표면CD11c분자표체，이증가세포표면CD80화CD86분자표체。세포표면CD80화CD86분자작위면역반응적중요협동자격분자재항원제정세포표면표체승고，칙격활T세포면역반응적능력증강。
Objective To explore the efficacy of LILRB2 siRNA on the expression of phenotype of CD11c, CD80, CD86 and its underlying meaning on mouse borrow dendritic cells (DC). Methods On the base of the routine culture, both the test group and the two control groups which were subdivided into void control group and control group were treated with 20 ng/ml GM-CSF and 20 ng/ml IL-4 to stimulate the growth of DC cells extracted from mouse bone marrow. At the fifth day, the test group was further transfected with LILRB2-siRNA, the void control group was transfected with empty plasmid, and the control group was added nothing but fluid media. After transfection for 72 h, all groups were observed under microscope and CD11c, CD80, CD86 were measured with flow cytometry. Results At the eighth day, the DC cells were all found under microcopy. Flow cytometry demonstrated there was no significant difference of the expression of CD11c among test group (0.662±0.174), void control group (0.675±0.237) and control group (0.688±0.076) (P>0.05). The expression of CD80 in test group (0.626±0.060) was higher than its expression in void control group (0.406±0.163) and control group (0.409±0.100) (P<0.05). The expression of CD86 in test group (0.730±0.102) was also higher than its expression in void control group (0.497±0.278) and control group (0.368±0.073) (P<0.05). Conclusions The application of LILRB2-siRNA would not alter the expression of CD11c on DC cells but effectively promote the phenotype molecules expression of CD80 and CD86, this often represents the enhancement capability of DC cells to stimulate the activation of T cells as the expression of CD80, CD86 on the APC cells are thought as key co-stimulatory molecules to facilitate this process.
