本文選題：Notch信號(hào)通路 + DAPT��； 參考：《中國(guó)病原生物學(xué)雜志》2014年12期

【摘要】：目的初步探索Notch信號(hào)對(duì)樹突狀細(xì)胞(dendritic cell,DC)介導(dǎo)的抗寄生蟲感染免疫反應(yīng)的影響。方法體外培養(yǎng)骨髓來(lái)源的小鼠DC細(xì)胞,利用γ-分泌酶抑制劑N-[N-(3,5-Difluorophenacetyl)-L-alanyl]-S-phenylglycine tbutyl ester,DAPT于不同時(shí)間段處理細(xì)胞,阻斷DC的Notch信號(hào)通路,培養(yǎng)第7d時(shí)收集DC,用細(xì)粒棘球蚴重組抗原鐵蛋白(ferritin protein of Echinococcus granulosus,Eg.ferritin)體外刺激DC,利用掃描電鏡觀察DC形態(tài)的改變,采用流式細(xì)胞術(shù)檢測(cè)DC表面分子MHCⅡ、CD40及CD80/CD86的表達(dá)情況。結(jié)果 DC細(xì)胞數(shù)量隨DAPT濃度的增高而降低;經(jīng)不同濃度DAPT于不同時(shí)間段處理后,DC細(xì)胞中Notch1mRNA的表達(dá)受到抑制,以50μmol/L DAPT在第0d處理DC,對(duì)Notch1mRNA的抑制效果更顯著(P0.05);Eg.ferritin和LPS均能刺激DC細(xì)胞表面樹突的生成及表面分子MHCⅡ、CD40及CD80/CD86的表達(dá),且Eg.ferritin比LPS的刺激作用更顯著(P0.05),而加入DAPT后,DC細(xì)胞表面樹突的生成減少,各表面分子的表達(dá)水平降低(P0.05),并削弱了Eg.ferritin和LPS的刺激作用。結(jié)論Eg.ferritin能促進(jìn)DC細(xì)胞的分化成熟,而阻斷Notch信號(hào)通路會(huì)影響DC細(xì)胞的分化成熟,并降低DC細(xì)胞對(duì)Eg.ferritin的反應(yīng)能力。其分子機(jī)制涉及Notch信號(hào)通路。
[Abstract]:Objective to investigate the effect of Notch signal on the immune response of dendritic cells to parasitic infection.Methods Murine DC cells derived from bone marrow were cultured in vitro, and the Notch signaling pathway of DC was blocked by N- [N-N- (N-H3) 5-Difluorophenacetyl-L-alanyl] -S-phenylglycine tbutyl esteresterDAPT at different time points.DCS were collected at the 7th day of culture. DCs were stimulated with ferritin protein of Echinococcus granulosus Eg.Ferritin in vitro. The morphological changes of DC were observed by scanning electron microscope. The expression of MHC 鈪，

本文編號(hào)：1737190