本文選題：信號(hào)轉(zhuǎn)導(dǎo)與轉(zhuǎn)錄活化因子 + 未成熟樹突狀細(xì)胞　； 參考：《免疫學(xué)雜志》2017年06期

【摘要】：目的研究過表達(dá)信號(hào)轉(zhuǎn)導(dǎo)與轉(zhuǎn)錄活化因子3(signal transducers and activators of transcription 3,STAT3)對(duì)未成熟樹突細(xì)胞(immature dendritic cells,im DC)抗分化能力的影響。方法分離獲取imDC細(xì)胞,分別加入TNF-α培養(yǎng)、空載病毒感染后加入TNF-α培養(yǎng)、p LVX-IRES-Zs Green1-STAT3慢病毒感染后加入TNF-α培養(yǎng)。流式細(xì)胞術(shù)鑒定細(xì)胞表面分子標(biāo)志物CD86/MHCⅡ的表達(dá)變化,Western blot檢測(cè)細(xì)胞免疫耐受因子IL-10、IDO、NF-κB的表達(dá)變化;掃描電鏡觀察細(xì)胞超微結(jié)構(gòu)變化,Transwell實(shí)驗(yàn)檢測(cè)細(xì)胞遷移能力。同種異體混合淋巴細(xì)胞反應(yīng)檢測(cè)對(duì)T淋巴細(xì)胞的刺激能力。結(jié)果與正常分化的imDC細(xì)胞相比,過表達(dá)STAT3的imDC細(xì)胞在TNF-α刺激后表面標(biāo)志分子CD86/MHCⅡ低表達(dá),NF-κB、IDO、IL-10蛋白的表達(dá)增強(qiáng),細(xì)胞形態(tài)與未分化時(shí)相似,其遷移能力較強(qiáng)、T淋巴細(xì)胞刺激能力明顯減弱。結(jié)論經(jīng)感染重組STAT3病毒的im DC細(xì)胞在TNF-α刺激下,仍能保持未分化狀態(tài)。
[Abstract]:Objective to investigate the effect of overexpression of signal transduction and transcription activator 3 (signal transducers and activators of transcription 3 / STAT3 on the differentiation of immature dendritic cells (immature dendritic cells). Methods imDC cells were isolated and cultured with TNF- 偽, and then infected with TNF- 偽. LVX-IRES-Zs Green1-STAT3 lentivirus was cultured with TNF- 偽 and LVX-IRES-Zs Green1-STAT3. Flow cytometry was used to identify the expression of CD86 / MHC 鈪，

本文編號(hào)：2084111