胶原诱导的关节炎小鼠髓样抑制细胞Arg-1、iNOS的mRNA表达  

Expression of Arg-1and iNOS mRNA in myeloid-derived suppressor cells(MDSC) from collagen-induced arthritis mice

作　　者：王瑞[1] 王文红[2] 朱波[1] 许秋桂 熊御云[1] 严佳婧 舒扬[1] 焦志军[1] 

机构地区：[1]江苏大学附属医院检验科中心实验室,镇江市医学免疫学重点实验室,镇江212001 [2]江苏大学医学院病原生物学系,镇江212013

出　　处：《现代免疫学》2015年第3期210-213,共4页Current Immunology

基　　金：国家自然科学基金资助项目(81172871;81373217);江苏省科技厅科技创新与成果转化(生命健康科技)专项资金(BL2012057);江苏大学大学生科研立项(13A237)

摘　　要：探讨胶原诱导的关节炎(collagen-induced arthritis,CIA)小鼠发病过程中骨髓和脾脏扩增的髓样抑制细胞(myeloidderived suppressor cells,MDSC)产物Arg-1、iNOS的mRNA表达水平。应用牛II型胶原免疫DBA/1J小鼠诱导CIA模型,在第一次免疫后的第45天,采用流式细胞术分选小鼠骨髓和脾脏CD11b+Gr-1+的MDSC(纯度>98%),利用定量RT-PCR技术检测MDSC产物Arg-1、iNOS的mRNA表达水平。结果发现,脾脏中,CIA小鼠MDSC细胞Arg-1mRNA表达低于正常小鼠,而iNOS mRNA表达高于正常小鼠,二者差异均具有统计学意义(P均<0.01)。CIA小鼠的骨髓MDSC细胞Arg-1mRNA表达低于正常小鼠,而iNOS mRNA表达高于正常小鼠,但差异均无统计学意义(P均>0.05)。上述结果提示CIA小鼠骨髓和脾脏中的MDSC可能通过产生高水平的iNOS参与CIA的发病。To explore the expression of Arg-1 and iNOS in the myeloid-derived suppressor cells from the bone marrow and spleen of mice with collagen-induced arthritis, DBA/1J mice were immunized with bovine type Ⅱ collagen to induce arthritis and MDSC were sorted by flow eytometry from CIA mice on day 45 after the initial immunization. The purity of sorted MDSC was〉 98%, as verified by flow cytometry. The expression levels of Arg-1 and iNOS mRNA was determined by quantitative real time polymerase chain reaction （qRT-PCR）. For the spleen, the expression of Arg-1 in MDSC from CIA mice was obviously lower than that in the normal mice, and iNOS expression was increased significantly compared with that in normal mice （both P〈0. 01）. Although the level of Arg-1 mRNA in the bone marrow MDSC from the CIA mice was less than that in the normal mice and the iNOS mRNA expression was higher than that in the normal mice, the differences were not statistically significant （both P〉0.05）. These findings suggest that MDSC in the bone marrow and spleen of CIA mice may regulate to the progression of the CIA through producing high levels of iNOS.

关 键 词：胶原诱导的关节炎 髓样抑制细胞 Arg-1 INOS 

分 类 号：R392.11[医药卫生—免疫学]