国际免疫学杂志
國際免疫學雜誌
국제면역학잡지
INTERNATIONAL JOURNAL OF IMMUNOLOGY
2015年
3期
199-202
,共4页
龚邦东%路臻豪%景波%黄家树%阮光峰%刘劼%汤建平
龔邦東%路臻豪%景波%黃傢樹%阮光峰%劉劼%湯建平
공방동%로진호%경파%황가수%원광봉%류할%탕건평
间充质干细胞%B细胞%微小核糖核酸155%肿瘤坏死因子-α
間充質榦細胞%B細胞%微小覈糖覈痠155%腫瘤壞死因子-α
간충질간세포%B세포%미소핵당핵산155%종류배사인자-α
Mesenchymal stem cells%B cells%MiRNA-155%Tumor necrosis factor-α
目的 研究间充质干细胞(MSCs)对小鼠活化B细胞微小核糖核酸155(miRNA-155)和肿瘤坏死因子-α(TNF-α)表达的影响,探讨MSCs对B细胞的调控机制.方法 以小鼠脾脏原代B细胞为研究模型,在B细胞受体(BCR)刺激下,与人脐带来源的MSCs共培养3d后,收集悬浮的B细胞,进行细胞计数,实时定量PCR检测B细胞miRNA-155和TNF-α mRNA水平,酶联免疫吸附试验(ELISA)法检测共培养上清中细胞因子免疫球蛋白G(IgG)、TNF-α、转化生长因子β(TGF-β)、前列腺素E2(PGE2)、白细胞介素(IL)-10和吲哚胺2,3-双加氧酶(IDO)水平.结果 B细胞活化后增殖明显,MSCs能轻微抑制B细胞增殖(F =5.39,P＜0.05).B细胞活化后miRNA-155和TNF-α mRNA均上调明显,MSCs能部分逆转miRNA-155和TNF-α mRNA的升高(F=18.85,P＜0.01和F=10.26,P＜0.05).B细胞活化后共培养上清TNF-α、IgG升高明显,MSCs能部分缓解TNF-α和IgG的升高(F=27.94,P＜0.01和F=4.81,P＜0.05).在MSCs和B细胞共培养上清中,PGE2升高尤为明显,其次是IDO.结论 MSC可能通过可溶性因子PGE2和IDO抑制活化B细胞miRNA-155和TNF-α的表达,MSCs可能通过抑制B细胞治疗免疫疾病发挥重要作用.
目的 研究間充質榦細胞(MSCs)對小鼠活化B細胞微小覈糖覈痠155(miRNA-155)和腫瘤壞死因子-α(TNF-α)錶達的影響,探討MSCs對B細胞的調控機製.方法 以小鼠脾髒原代B細胞為研究模型,在B細胞受體(BCR)刺激下,與人臍帶來源的MSCs共培養3d後,收集懸浮的B細胞,進行細胞計數,實時定量PCR檢測B細胞miRNA-155和TNF-α mRNA水平,酶聯免疫吸附試驗(ELISA)法檢測共培養上清中細胞因子免疫毬蛋白G(IgG)、TNF-α、轉化生長因子β(TGF-β)、前列腺素E2(PGE2)、白細胞介素(IL)-10和吲哚胺2,3-雙加氧酶(IDO)水平.結果 B細胞活化後增殖明顯,MSCs能輕微抑製B細胞增殖(F =5.39,P＜0.05).B細胞活化後miRNA-155和TNF-α mRNA均上調明顯,MSCs能部分逆轉miRNA-155和TNF-α mRNA的升高(F=18.85,P＜0.01和F=10.26,P＜0.05).B細胞活化後共培養上清TNF-α、IgG升高明顯,MSCs能部分緩解TNF-α和IgG的升高(F=27.94,P＜0.01和F=4.81,P＜0.05).在MSCs和B細胞共培養上清中,PGE2升高尤為明顯,其次是IDO.結論 MSC可能通過可溶性因子PGE2和IDO抑製活化B細胞miRNA-155和TNF-α的錶達,MSCs可能通過抑製B細胞治療免疫疾病髮揮重要作用.
목적 연구간충질간세포(MSCs)대소서활화B세포미소핵당핵산155(miRNA-155)화종류배사인자-α(TNF-α)표체적영향,탐토MSCs대B세포적조공궤제.방법 이소서비장원대B세포위연구모형,재B세포수체(BCR)자격하,여인제대래원적MSCs공배양3d후,수집현부적B세포,진행세포계수,실시정량PCR검측B세포miRNA-155화TNF-α mRNA수평,매련면역흡부시험(ELISA)법검측공배양상청중세포인자면역구단백G(IgG)、TNF-α、전화생장인자β(TGF-β)、전렬선소E2(PGE2)、백세포개소(IL)-10화신타알2,3-쌍가양매(IDO)수평.결과 B세포활화후증식명현,MSCs능경미억제B세포증식(F =5.39,P＜0.05).B세포활화후miRNA-155화TNF-α mRNA균상조명현,MSCs능부분역전miRNA-155화TNF-α mRNA적승고(F=18.85,P＜0.01화F=10.26,P＜0.05).B세포활화후공배양상청TNF-α、IgG승고명현,MSCs능부분완해TNF-α화IgG적승고(F=27.94,P＜0.01화F=4.81,P＜0.05).재MSCs화B세포공배양상청중,PGE2승고우위명현,기차시IDO.결론 MSC가능통과가용성인자PGE2화IDO억제활화B세포miRNA-155화TNF-α적표체,MSCs가능통과억제B세포치료면역질병발휘중요작용.
Objective To study the effects of mesenchymal stem cells (MSCs) on the microRNA-155 (miRNA-155) and tumor necrosis factor-α(TNF-α) of activated B cells,and explore the regulation mechanisms of MSCs on B cells.Methods We used primary B cells from mouse spleen as the research models.B cells were co-cultured with human umbilical cord derived MSCs for three days in the B-cell receptor (BCR) stimulation.The suspension cells were collected and counted.Real-time PCR was used to determine the miRNA-155 and TNF-α mRNA levels in B cells.Enzyme-linked immunosorbent assay (ELISA) was used to inspect supernatant immunoglobulin G (IgG) and cytokines including TNF-α,transforming growth factor (TGF-β),prostaglandin E2 (PGE2),interleukin-10 (IL-10),and indoleamine 2,3-dioxygenase (IDO).Results B cells showed significant proliferation after activation,which can be slightly inhibited by MSCs (F =5.39,P ＜0.05).MiRNA-155 and TNF-o mRNA in B cells were significantly upregulated after B-cell activation,which can be partially reversed by MSCs (F =18.85,P ＜ 0.01 and F =10.26,P ＜ 0.05).TNF-α and IgG in co-culture supernatant were significantly increased after B cell activation,and MSCs can partially alleviate the elevated TNF-α and IgG (F =27.94,P ＜ 0.01 and F =4.81,P ＜ 0.05).In co-culture supernatants,PGE2 increasesd markedly,followed by IDO.Conclusion MSC can downregulate miRNA-155 and TNF-α expression in activated B cells possibly via PGE2 or IDO.This might play some important role in MSC treatment for immune disorders.
