【摘要】 目的:探讨胶原诱导性关节炎(CIA)小鼠炎症条件下,诱导的调节性T细胞(i Tregs)与B细胞的相互作用模式。方法:分别从正常DBA1/J和免疫后第35天的关节炎小鼠的脾脏细胞分选出CD19+细胞(N-B和CIA-B细胞),以此细胞作为抗原提呈细胞观察其诱导Tregs生成的差异;经典方法制备i Tregs,将CIA-B细胞与i Tregs共培养,观察其对i Tregs自身的增殖及i Tregs表达CTLA-4的影响;观察i Tregs对CIA-B细胞共刺激分子(CD80,CD86)和MHCⅡ类分子表达的影响,并设立Transwell实验探讨作用机制。结果:CIA-B较N-B诱导更多Tregs的生成;CIA-B促进i Tregs的增殖并上调i Tregs细胞表面CTLA-4的表达,后者的作用是通过细胞直接接触的途径实现;同时,i Tregs促进CIA-B细胞表面共刺激分子和MHCⅡ类分子的表达且该作用也通过细胞直接接触途径而实现。结论:在CIA炎症条件下,i Tregs通过与B细胞的相互作用来发挥其免疫抑制作用,两者的相互作用通过细胞直接接触实现。更多还原

【Abstract】 Objective:To investigate the interactions between induced T regulatory cells(i Tregs) and B cells in the inflammatory milieu in mice with collagen-induced arthritis(CIA).Methods:CD19+cells were isolated from the spleen cells of normal DBA1/J(N-B) mice and CIA mice(CIA-B) on the 35 th day after the first immunization with established arthritis.These B cells were used as antigen-presenting cells to observe their effects on the induction of Tregs.Tregs were induced with the classic method and co-cultured with CIA-B cells.CIA-B cell effects on i Treg proliferation and the expression of CTLA-4 on i Tregs were explored.i Tregs’ influence on the expressions of co-stimulators(CD80,CD86) and MHCⅡ on B cells was studied and its mechanism was determined by the Transwell experiments.Results:CIA-B could induce more Treg production and proliferation.CIA-B could also promote the CTLA-4 expression on i Treg cell surface which worked through a cell-contact pathway,while i Tregs could increase the expressions of co-stimulators(CD80,CD86) and MHCⅡ by the same way.Conclusion:i Tregs could show their immune suppressive function through the interactions with CIA-B cells in the inflammatory milieu in mice with CIA.These interactions work by a cell-contact pathway.更多还原