摘要
目的 :研究CD4 + CD2 5 + Treg细胞对诱导小鼠实验性自身免疫性甲状腺炎 (EAT)的影响。方法 :磁性细胞分离器 (MACS)分离CD4 + CD2 5 + T细胞 ,通过体外细胞增殖试验和IFN γ的测定研究CD4 + CD2 5 + T细胞对CD4 + CD2 5 - T细胞的免疫抑制作用 ,同时通过过继转移试验研究CD4 + CD2 5 + T细胞抑制小鼠EAT的发生。结果 :MACS分离的CD4 + CD2 5 + T细胞纯度可达到 85 %～ 94 % ,特异性表达FoxP3基因 ,体外能明显抑制效应性T细胞的增殖和IFN γ的产生 ;将CD4 + CD2 5 + T细胞与病理性CD2 5 - T细胞共同注射正常小鼠 ,可抑制病理性T细胞诱导EAT的发生。结论 :CD4 + CD2 5 +
Objective:To investigate the immunosuppression of mouse CD4^+CD25^+ regulatory T (Treg) cell.Methods:Mouse CD4^+CD25^+T cells were isolated by MACS (magnetic cell sorting)and identified by FCM(flow cytometry). Their suppression on the proliferation and the IFN-γ production of CD4^+CD25^-T effector cell were analyzed by cell proliferation assay and ELISA, respectively. The effects of CD4^+CD25^+T cells on the preventing experimental autoimmune thyroiditis were assessed by adoptive transfer.Results:CD4^+CD25^+T cell can be successfully classified by MACS with the purity reaching 85%～94% and specifically express the FoxP3 gene which is the ‘master control gene’ for Treg cells. These cells could suppressive the proliferation and the IFN-γ production of CD4^+CD25^-T effector cells in vitro. Co-transfer of CD4^+CD25^+T cell could prevent adoptive transfer of experimental autoimmune thyroiditis by pathogenic CD25^-T cell in vivo.Conclusion:CD4^+CD25^+ Treg contribute notably to regulation effector T cell and protection from autoimmune disease.
出处
《中国免疫学杂志》
CAS
CSCD
北大核心
2005年第2期102-104,107,共4页
Chinese Journal of Immunology
基金
国家自然科学基金 (3 0 3 0 0 169)
江苏省自然科学基金 (BK2 0 0 44 0 5 )资助
