国际免疫学杂志
國際免疫學雜誌
국제면역학잡지
INTERNATIONAL JOURNAL OF IMMUNOLOGY
2014年
5期
449-452
,共4页
唐春莲%郭思洁%杨进%祝青%刘晓宏
唐春蓮%郭思潔%楊進%祝青%劉曉宏
당춘련%곽사길%양진%축청%류효굉
日本血吸虫%CD4+ CD25+调节性T细胞%γ-干扰素%白细胞介素-4%白细胞介素-5%白细胞介素-10
日本血吸蟲%CD4+ CD25+調節性T細胞%γ-榦擾素%白細胞介素-4%白細胞介素-5%白細胞介素-10
일본혈흡충%CD4+ CD25+조절성T세포%γ-간우소%백세포개소-4%백세포개소-5%백세포개소-10
Schistosoma.japonicum%CD4+ CD25+ regulatory T cells%γ-interferon%Interleukin-4%Interleukin-5%Interleukin-10
目的 探讨CD4+ CD25+调节性T细胞(Tregs)在日本血吸虫免疫逃避中的作用及其机制.方法 雌性BALB/c小鼠随机分成3组,即正常对照组、感染对照组和抗CD25单克隆抗体(anti-CD25 mAb)组,各感染组每只小鼠均经腹部皮肤感染日本血吸虫尾蚴40条,感染后两周anti-CD25 mAb组每只小鼠经腹腔注射anti-CD25 mAb 300 μg,其它组注射等体积的PBS,感染后5周杀鼠冲虫,计数每只小鼠虫荷.收集脾细胞及培养上清,流式细胞术检测脾淋巴细胞中CD4+ CD25+ Tregs百分比.双抗夹心ELISA法测定脾细胞培养上清中的γ-干扰素(IFN-γ)、IL-4、IL-5、IL-10的含量.结果 Anti-CD25mAb组虫荷(23.17 ±6.94)明显低于感染对照组[(30.17 ±5.85),P=0.047];感染对照组脾淋巴细胞中CD4+ CD25+ Tregs百分比(2.68 ±0.12)％明显高于正常对照组[(1.98±0.33％),P=0.049],而anti-CD25mAb组脾淋巴细胞中CD4+ CD25+ Tregs百分比(1.28±0.30)％明显低于感染对照组(P=0.000);anti-CD25mAb组脾细胞培养上清中IFN-γ的含量(386.87±24.85) pg/mL明显高于感染对照组[(61.32±8.75) pg/mL,P=0.000],其余细胞因子组间无统计学意义.结论 anti-CD25 mAb能部分封闭CD4+ CD25+ Tregs后有利于机体清除日本血吸虫,其机制可能为增强Th1型免疫反应,宿主CD4+ CD25+ Tregs有助于日本血吸虫逃避宿主的免疫攻击.
目的 探討CD4+ CD25+調節性T細胞(Tregs)在日本血吸蟲免疫逃避中的作用及其機製.方法 雌性BALB/c小鼠隨機分成3組,即正常對照組、感染對照組和抗CD25單剋隆抗體(anti-CD25 mAb)組,各感染組每隻小鼠均經腹部皮膚感染日本血吸蟲尾蚴40條,感染後兩週anti-CD25 mAb組每隻小鼠經腹腔註射anti-CD25 mAb 300 μg,其它組註射等體積的PBS,感染後5週殺鼠遲蟲,計數每隻小鼠蟲荷.收集脾細胞及培養上清,流式細胞術檢測脾淋巴細胞中CD4+ CD25+ Tregs百分比.雙抗夾心ELISA法測定脾細胞培養上清中的γ-榦擾素(IFN-γ)、IL-4、IL-5、IL-10的含量.結果 Anti-CD25mAb組蟲荷(23.17 ±6.94)明顯低于感染對照組[(30.17 ±5.85),P=0.047];感染對照組脾淋巴細胞中CD4+ CD25+ Tregs百分比(2.68 ±0.12)％明顯高于正常對照組[(1.98±0.33％),P=0.049],而anti-CD25mAb組脾淋巴細胞中CD4+ CD25+ Tregs百分比(1.28±0.30)％明顯低于感染對照組(P=0.000);anti-CD25mAb組脾細胞培養上清中IFN-γ的含量(386.87±24.85) pg/mL明顯高于感染對照組[(61.32±8.75) pg/mL,P=0.000],其餘細胞因子組間無統計學意義.結論 anti-CD25 mAb能部分封閉CD4+ CD25+ Tregs後有利于機體清除日本血吸蟲,其機製可能為增彊Th1型免疫反應,宿主CD4+ CD25+ Tregs有助于日本血吸蟲逃避宿主的免疫攻擊.
목적 탐토CD4+ CD25+조절성T세포(Tregs)재일본혈흡충면역도피중적작용급기궤제.방법 자성BALB/c소서수궤분성3조,즉정상대조조、감염대조조화항CD25단극륭항체(anti-CD25 mAb)조,각감염조매지소서균경복부피부감염일본혈흡충미유40조,감염후량주anti-CD25 mAb조매지소서경복강주사anti-CD25 mAb 300 μg,기타조주사등체적적PBS,감염후5주살서충충,계수매지소서충하.수집비세포급배양상청,류식세포술검측비림파세포중CD4+ CD25+ Tregs백분비.쌍항협심ELISA법측정비세포배양상청중적γ-간우소(IFN-γ)、IL-4、IL-5、IL-10적함량.결과 Anti-CD25mAb조충하(23.17 ±6.94)명현저우감염대조조[(30.17 ±5.85),P=0.047];감염대조조비림파세포중CD4+ CD25+ Tregs백분비(2.68 ±0.12)％명현고우정상대조조[(1.98±0.33％),P=0.049],이anti-CD25mAb조비림파세포중CD4+ CD25+ Tregs백분비(1.28±0.30)％명현저우감염대조조(P=0.000);anti-CD25mAb조비세포배양상청중IFN-γ적함량(386.87±24.85) pg/mL명현고우감염대조조[(61.32±8.75) pg/mL,P=0.000],기여세포인자조간무통계학의의.결론 anti-CD25 mAb능부분봉폐CD4+ CD25+ Tregs후유리우궤체청제일본혈흡충,기궤제가능위증강Th1형면역반응,숙주CD4+ CD25+ Tregs유조우일본혈흡충도피숙주적면역공격.
Objective To explore the effect and mechanism of CD4 + CD25 + Tregs in S.japonicum immune evasion.Methods Female BALB/c mice were randomly divided into normal control group,infected control and anti-CD25 mAb group.Each mouse was infected percutaneously with 40 S.japonicum cercaria.After 2 weeks infection,anti-CD25 mAb group was injected intraperitoneal with 300 μg anti-CD25 mAb each mouse.After 5 weeks infection,all mice were succumbed to measure worm burden.The percent of CD4+ CD25 + Tregs in spleen was measured with flow cytometer.The expression of gamma interferon (IFN-γ),interleukin-4 (IL-4),interleukin-5 (IL-5) and interleukin-10 (IL-10) in cultural suspension of splenic cells was detected by sandwich-ELISA after stimulation with ConA.Results Worm burden in anti-CD25 mAb group (23.17 ± 6.94) was extremely lower than in infected control group [(30.17 ± 5.85) pg/mL,P =0.047].Compared to those of normal [(1.98 ±0.33),P =0.049] and infected control group [(2.68 ±0.12),P =0.000],the ration of CD4+ CD25+ Tregs were extremely low in anti-CD25 mAb group (1.28 ± 0.30).The level of IFN-γ in anti-CD25 mAb group [(386.87 ± 24.85) pg/mL,P =0.000] was extremely higher than that of infected control group (61.32 ± 8.75)pg/mL,while the levels of IL-4,IL-5 and IL-10 were not significant different among the three groups.Conclusion These results hint that CD4+ CD25+ Tregs contribute to the escape of S.japonicum from the host immune assault,while anti-CD25 mAb can partially block CD4+ CD25+ Tregs and favor the host to clear parasite by enhancing Th1-type immune response.
