国际呼吸杂志
國際呼吸雜誌
국제호흡잡지
INTERNATIONAL JOURNAL OF RESPIRATION
2011年
3期
173-176
,共4页
王彦%王长征%林科雄%夏俊波
王彥%王長徵%林科雄%夏俊波
왕언%왕장정%림과웅%하준파
树突状细胞%共刺激分子%过敏原%免疫耐受
樹突狀細胞%共刺激分子%過敏原%免疫耐受
수돌상세포%공자격분자%과민원%면역내수
Dendritic cell%Co-stimulatory molecule%Allergen%Immune tolerance
目的 观察不同浓度屋尘螨(HDM)对HDM过敏原Der p2基因修饰的树突状细胞(DC)表面分子的影响.方法 以未转染DC为对照,不同浓度HDM处理HDM主要抗原基因Der p2转染的DC(Der p2-DC),培养72 h后流式细胞仪检测Der p2 DC表面共刺激分子CD80、CD86和MHCⅡ.结果 加入HDM后,无论浓度高低,与未加入HDM相比,Der p2-DC表面分子CD80、CD86和MHCⅡ阳性表达率均无显著变化.而加入HDM后,未转染DC表面分子CD80、CD86和MHCⅡ阳性表达率与未加入HDM相比均显著升高.结论 特异性过敏原刺激不能增强过敏原基因修饰DC表面共刺激分子的表达.
目的 觀察不同濃度屋塵螨(HDM)對HDM過敏原Der p2基因脩飾的樹突狀細胞(DC)錶麵分子的影響.方法 以未轉染DC為對照,不同濃度HDM處理HDM主要抗原基因Der p2轉染的DC(Der p2-DC),培養72 h後流式細胞儀檢測Der p2 DC錶麵共刺激分子CD80、CD86和MHCⅡ.結果 加入HDM後,無論濃度高低,與未加入HDM相比,Der p2-DC錶麵分子CD80、CD86和MHCⅡ暘性錶達率均無顯著變化.而加入HDM後,未轉染DC錶麵分子CD80、CD86和MHCⅡ暘性錶達率與未加入HDM相比均顯著升高.結論 特異性過敏原刺激不能增彊過敏原基因脩飾DC錶麵共刺激分子的錶達.
목적 관찰불동농도옥진만(HDM)대HDM과민원Der p2기인수식적수돌상세포(DC)표면분자적영향.방법 이미전염DC위대조,불동농도HDM처리HDM주요항원기인Der p2전염적DC(Der p2-DC),배양72 h후류식세포의검측Der p2 DC표면공자격분자CD80、CD86화MHCⅡ.결과 가입HDM후,무론농도고저,여미가입HDM상비,Der p2-DC표면분자CD80、CD86화MHCⅡ양성표체솔균무현저변화.이가입HDM후,미전염DC표면분자CD80、CD86화MHCⅡ양성표체솔여미가입HDM상비균현저승고.결론 특이성과민원자격불능증강과민원기인수식DC표면공자격분자적표체.
Objective To investigate the effects of house dust mites (HDM) with diverse concentrations on the expressions of co-stimulatory molecules of HDM major antigen gene Der p2 modified dendritic cell(DC). Methods Der p2 gene modified DC(Der p2-DC) and control DC(non-transfected DC)were treated 72 h by H DM with diverse concentrations respectively. The expressions of CD80,CD86 and MHC Ⅱ ,the surface co-stimulatory molecules on Der p2-DC and control DC, were detected by FACS.Results FACS analysis showed that positive expression percentages of CD80,CD86 and MHC Ⅱ on Der p2-DC treated with HDM had no significant change,compared with Der p2-DC treated without HDM.After treated with HDM, positive expression percentages of CD80, CD86 and MHC Ⅱ on control DC increased significantly. Conclusions Specific allergen pulsing could not increase the expressions of costimulatory molecules of allergen gene modified DC.