细胞与分子免疫学杂志
細胞與分子免疫學雜誌
세포여분자면역학잡지
2009年
10期
894-896
,共3页
欧阳清%陈琨%王曦%张春梅%郭俊%魏玉英%孙元杰%徐竹蔚%杨琨
歐暘清%陳琨%王晞%張春梅%郭俊%魏玉英%孫元傑%徐竹蔚%楊琨
구양청%진곤%왕희%장춘매%곽준%위옥영%손원걸%서죽위%양곤
NKT细胞%EAE%免疫调节
NKT細胞%EAE%免疫調節
NKT세포%EAE%면역조절
NKT cell%EAE%immunoregulation
目的:观察NKT细胞在实验性自身免疫性脑脊髓炎(EAE)小鼠脾脏和肝脏中所占百分比的变化特点,探讨NKT细胞在EAE模型中的免疫调节作用.方法:以MOG_(35-55)21肽诱导C57BL/6小鼠建立EAE模型并进行临床评分.于发病高峰期处死小鼠,分离脾脏和肝脏淋巴细胞,采用免疫荧光染色和流式细胞术(FCM)分析,观察EAE小鼠与正常小鼠脾脏和肝脏中NKT细胞在全部淋巴细胞中所占百分率的变化.结果:在EAE小鼠不同器官中,NKT细胞占淋巴细胞的百分率均较正常小鼠减少.脾脏NKT细胞百分率(%)从正常组2.22±0.14下降到EAE模型组1.94±0.07(P<0.05),肝脏NKT细胞百分率(%)从正常组5.52±2.17下降到2.67±1.41(P<0.05).结论:NKT细胞在EAE模型C57BL/6小鼠脾脏和肝脏中增殖受抑,提示EAE发病可能通过对NKT细胞数量的调节进而影响其对免疫应答的调节.
目的:觀察NKT細胞在實驗性自身免疫性腦脊髓炎(EAE)小鼠脾髒和肝髒中所佔百分比的變化特點,探討NKT細胞在EAE模型中的免疫調節作用.方法:以MOG_(35-55)21肽誘導C57BL/6小鼠建立EAE模型併進行臨床評分.于髮病高峰期處死小鼠,分離脾髒和肝髒淋巴細胞,採用免疫熒光染色和流式細胞術(FCM)分析,觀察EAE小鼠與正常小鼠脾髒和肝髒中NKT細胞在全部淋巴細胞中所佔百分率的變化.結果:在EAE小鼠不同器官中,NKT細胞佔淋巴細胞的百分率均較正常小鼠減少.脾髒NKT細胞百分率(%)從正常組2.22±0.14下降到EAE模型組1.94±0.07(P<0.05),肝髒NKT細胞百分率(%)從正常組5.52±2.17下降到2.67±1.41(P<0.05).結論:NKT細胞在EAE模型C57BL/6小鼠脾髒和肝髒中增殖受抑,提示EAE髮病可能通過對NKT細胞數量的調節進而影響其對免疫應答的調節.
목적:관찰NKT세포재실험성자신면역성뇌척수염(EAE)소서비장화간장중소점백분비적변화특점,탐토NKT세포재EAE모형중적면역조절작용.방법:이MOG_(35-55)21태유도C57BL/6소서건립EAE모형병진행림상평분.우발병고봉기처사소서,분리비장화간장림파세포,채용면역형광염색화류식세포술(FCM)분석,관찰EAE소서여정상소서비장화간장중NKT세포재전부림파세포중소점백분솔적변화.결과:재EAE소서불동기관중,NKT세포점림파세포적백분솔균교정상소서감소.비장NKT세포백분솔(%)종정상조2.22±0.14하강도EAE모형조1.94±0.07(P<0.05),간장NKT세포백분솔(%)종정상조5.52±2.17하강도2.67±1.41(P<0.05).결론:NKT세포재EAE모형C57BL/6소서비장화간장중증식수억,제시EAE발병가능통과대NKT세포수량적조절진이영향기대면역응답적조절.
AIM: To observe the changes of the number of NKT cells in spleens and livers of induced model of experimental autoimmune encephalomyelitis (EAE), and to study the role NKT cells play in the immunoregulation of EAE. METHODS: C57BL/6 mice were immunized with MOG<,35-55> peptide and received clinical evaluation daily. The mice were sacrificed at the fastigium and the splenic and hepatic lymphocytes were isolated. The changes of NKT cells in normal and EAE C57BL/6 mice were detected by flow cytometry. RESULTS: The percent of NKT cells in lymphocytes of different organs of EAE model were greater decreased than in that of normal mice. The percent of NKT cells in splenic lymphocytes of normal mice was 2.22± 0.14, while that in EAE mice was 1.94±0.07 (P < 0.05). The percent of NKI cells in hepatic lymphocytes of normal mice was 5.52±2.17, while that in EAE mice was 2.67± 1.41 (P < 0.05). CONCLUSION: The proliferation of splenic and hepatic NKT cells in C57BL/6 mice are inhibited in EAE model, which may indicate that the immune function conducted by NKT cell is down regulated in EAE mice.