中华微生物学和免疫学杂志
中華微生物學和免疫學雜誌
중화미생물학화면역학잡지
CHINESE JOURNAL OF MICROBIOLOGY AND IMMUNOLOGY
2009年
7期
592-596
,共5页
糖皮质激素%地塞米松%IL-2%调节性T细胞%细胞增殖
糖皮質激素%地塞米鬆%IL-2%調節性T細胞%細胞增殖
당피질격소%지새미송%IL-2%조절성T세포%세포증식
Glucocorticoid%Dexamethasone%IL-2%Regulatory T cells%Cell proliferation
目的 建立糖皮质激素联合IL-2选择性提高调节T细胞(Tr)/效应T细胞(Te)比例的方法,观察其对异基因抗原反应的抑制效应.方法 体内使用地塞米松(DxM,5 mg·kg-1·d-1)和IL-2(300 000 IU/d)处理C57BL/6N3d后提取脾单个核细胞(MNC);流式细胞仪(FCM)分析CD4+CD25+、cD25+Foxp3+等的变化.取经IL-2和DXM联合处理后第10天的C57BL/6N脾细胞,用BALB/c小鼠脾细胞作为异基因抗原对其进行刺激,测定其增殖反应.结果 经过糖皮质激素和IL-2联合处理,C57BL/6N鼠脾CD4+Cd2525Foxo3+Tr数量明显增加,DXM+IL-2组CD4+中CD25+Foxp3+Tr比例为24.22%±7.60%,与对照组相比(4.02%±0.84%)差异具有统计学意义(P=0.01).DXM+IL-2组供鼠Tr与Te之比显著上升(0.43±0.15),与对照组(0.14±0.01)相比,差异具有统计学意义(P=0.01).DXM+IL-2组表达更强的糖皮质激素诱导肿瘤坏死因子受体(GTTR),该组小鼠T细胞体外异基因抗原增殖反应明显减低(P<0.05).结论 DXM联合IL-2体内应用有效提高Ir/Te比例,抑制异基因抗原增殖反应.
目的 建立糖皮質激素聯閤IL-2選擇性提高調節T細胞(Tr)/效應T細胞(Te)比例的方法,觀察其對異基因抗原反應的抑製效應.方法 體內使用地塞米鬆(DxM,5 mg·kg-1·d-1)和IL-2(300 000 IU/d)處理C57BL/6N3d後提取脾單箇覈細胞(MNC);流式細胞儀(FCM)分析CD4+CD25+、cD25+Foxp3+等的變化.取經IL-2和DXM聯閤處理後第10天的C57BL/6N脾細胞,用BALB/c小鼠脾細胞作為異基因抗原對其進行刺激,測定其增殖反應.結果 經過糖皮質激素和IL-2聯閤處理,C57BL/6N鼠脾CD4+Cd2525Foxo3+Tr數量明顯增加,DXM+IL-2組CD4+中CD25+Foxp3+Tr比例為24.22%±7.60%,與對照組相比(4.02%±0.84%)差異具有統計學意義(P=0.01).DXM+IL-2組供鼠Tr與Te之比顯著上升(0.43±0.15),與對照組(0.14±0.01)相比,差異具有統計學意義(P=0.01).DXM+IL-2組錶達更彊的糖皮質激素誘導腫瘤壞死因子受體(GTTR),該組小鼠T細胞體外異基因抗原增殖反應明顯減低(P<0.05).結論 DXM聯閤IL-2體內應用有效提高Ir/Te比例,抑製異基因抗原增殖反應.
목적 건립당피질격소연합IL-2선택성제고조절T세포(Tr)/효응T세포(Te)비례적방법,관찰기대이기인항원반응적억제효응.방법 체내사용지새미송(DxM,5 mg·kg-1·d-1)화IL-2(300 000 IU/d)처리C57BL/6N3d후제취비단개핵세포(MNC);류식세포의(FCM)분석CD4+CD25+、cD25+Foxp3+등적변화.취경IL-2화DXM연합처리후제10천적C57BL/6N비세포,용BALB/c소서비세포작위이기인항원대기진행자격,측정기증식반응.결과 경과당피질격소화IL-2연합처리,C57BL/6N서비CD4+Cd2525Foxo3+Tr수량명현증가,DXM+IL-2조CD4+중CD25+Foxp3+Tr비례위24.22%±7.60%,여대조조상비(4.02%±0.84%)차이구유통계학의의(P=0.01).DXM+IL-2조공서Tr여Te지비현저상승(0.43±0.15),여대조조(0.14±0.01)상비,차이구유통계학의의(P=0.01).DXM+IL-2조표체경강적당피질격소유도종류배사인자수체(GTTR),해조소서T세포체외이기인항원증식반응명현감저(P<0.05).결론 DXM연합IL-2체내응용유효제고Ir/Te비례,억제이기인항원증식반응.
Objective To established the method of increasihg the proportion of T regulatory cells(Tr) to T effector cells(Te), which could suppresses allogeneic ahtigen reaction, by in vivo of glucocorti-coid (dexamethasone, DXM) combined with IL-2. Methods After combined treatment to male C57BL/6N mice (donor) with DXM(5 mg. kg-1· d-1 ) and IL-2 (300 000 IU · mouse-1·d-1) for 3 d, spleen mono-nuclear cells were made and were carried out by flow cytometry analysis. Using the spleen cells of BALB/c mice as aliogeneic antigen to stimulate the spleen cells of male C57BL/6N mice for 7 d after combined treat-ment of glucoeorticoid and IL-2, the reaction of cell proliferation was detected. Results After the treatrment of DXM and IL-2, CD4+ CD25+ Foxp3+ Tr cells in the spleen of C57BL/6N mice increased abviously. The ratio of CD25+ Foxp3+ Tr to CD4+ T cells was 24.22%±7.60% in the group of DXM combined with IL-2, while the control group was 4.02% ±0. 84% ( P =0. 01 ). Compared with the control group (0. 14±0.01 ), the ratio of Tr to Te increased obviously in the group of DXM combined with IL-2 (0.43±0. 15 ) ( P = 0.01 ). The group of DXM combined with IL-2 also expressed more glucocorticoid-induced tumor necrosis factor receptor(GITR) and alloreaction was suppressed/n vitro obviously ( P < 0. 05 ). Conclusion DXM amplifies IL-2 induced the proportion of Tr to Te, and suppresses the cell proliferation stimulated by alloge-neic antigen.
