鈣/鈣調(diào)素依賴性蛋白激酶Ⅱ和MHC Ⅱ類分子對(duì)TLR觸發(fā)的巨噬細(xì)胞與樹突狀細(xì)胞天然免疫應(yīng)答反應(yīng)的調(diào)控及其機(jī)制研究
發(fā)布時(shí)間：2022-01-26 15:50
Toll樣受體（Toll-like receptors, TLRs）作為一類重要的模式識(shí)別受體（Pattern recognition receptors, PRRs）主要表達(dá)于巨噬細(xì)胞和樹突狀細(xì)胞（Dendritic cells, DCs）表面,選擇性地識(shí)別病原體相關(guān)分子模式（Pathogen-associated molecular patterns, PAMPs）,構(gòu)成機(jī)體免疫系統(tǒng)抵御病原體入侵的第一道屏障。TLR是一類在各種生物體內(nèi)高度保守的I型跨膜蛋白,目前已在哺乳動(dòng)物中發(fā)現(xiàn)并克隆了12種。一旦識(shí)別了病原體中特定的分子結(jié)構(gòu),TLR就會(huì)激活其下游一系列的信號(hào)通路,活化天然免疫細(xì)胞產(chǎn)生炎性細(xì)胞因子和I型干擾素。TLR不僅啟動(dòng)天然免疫應(yīng)答,控制炎癥反應(yīng)的性質(zhì)、強(qiáng)度和持續(xù)時(shí)間,還可以通過(guò)上調(diào)DC表面的MHC II類分子和共刺激分子,促進(jìn)DC的成熟,指導(dǎo)抗原特異的免疫應(yīng)答尤其是Th1型反應(yīng)的產(chǎn)生,調(diào)節(jié)獲得性免疫應(yīng)答的強(qiáng)度和類型,成為連接初始免疫應(yīng)答和獲得性免疫應(yīng)答的橋梁。TLR信號(hào)過(guò)度活化或活化不足會(huì)導(dǎo)致機(jī)體功能異常和疾病的發(fā)生。許多的其他信號(hào)通路參與對(duì)TLR信號(hào)的嚴(yán)密調(diào)控。因此,對(duì)T...
【文章來(lái)源】：中國(guó)人民解放軍海軍軍醫(yī)大學(xué)上海市 211工程院校
【文章頁(yè)數(shù)】：111 頁(yè)
【學(xué)位級(jí)別】：博士
【部分圖文】：
干擾RAW264.7細(xì)胞中CaMKII的表達(dá)能抑制LPS觸發(fā)的炎性細(xì)胞因子和I型干擾素的產(chǎn)生Figure1-2.SilencingofCaMKIIexpressionattenuatesTLR4-activatedproinflammatorycytokineandtypeIinterferonproductioninRAW264.7cells.
圖 1-3. 干擾小鼠腹腔巨噬細(xì)胞中 CaMKII 的表達(dá)能抑制 TLR3、4、9 促發(fā)的炎性細(xì)胞因子和 I 型干擾素的產(chǎn)生Figure 1-3. Silencing of CaMKII expression attenuates TLR4,9,3-activatedproinflammatory cytokine and type I interferon production in macrophages.Mouse peritoneal macrophages (4 × 105) were transfected with control small RNA (Ctrl)or CaMKII-α siRNA1. After 48 hr, cells were stimulated with 0.1 μg/ml LPS (A), 0.3μM CpG ODN (B) or 10 μg/ml Poly(I:C) (C) for the indicated time. IL-6, TNF-α orIFN-β in the supernatants was measured by ELISA. Data are shown as mean ± SD ofthree independent experiments. **, P < 0.01.
CaMKII 能消除 CaMKII-α siRNA 對(duì) LP生的抑制α overexpression rescues CaMKII-α silenction in LPS-stimulated macrophages.d RAW264.7 cells were transfected withfter 36 hr, CaMKII-α and β-actin exprelot. Similar results were obtained in three inls (1.5 × 105) were transfected with contrAfter 36h, the cells were transfected withours later, the cells were stimulated with B) and IFN-β (C) in the supernatants wean ± SD of three independent experiments.
本文編號(hào)：3610756
【文章來(lái)源】：中國(guó)人民解放軍海軍軍醫(yī)大學(xué)上海市 211工程院校
【文章頁(yè)數(shù)】：111 頁(yè)
【學(xué)位級(jí)別】：博士
【部分圖文】：
干擾RAW264.7細(xì)胞中CaMKII的表達(dá)能抑制LPS觸發(fā)的炎性細(xì)胞因子和I型干擾素的產(chǎn)生Figure1-2.SilencingofCaMKIIexpressionattenuatesTLR4-activatedproinflammatorycytokineandtypeIinterferonproductioninRAW264.7cells.
圖 1-3. 干擾小鼠腹腔巨噬細(xì)胞中 CaMKII 的表達(dá)能抑制 TLR3、4、9 促發(fā)的炎性細(xì)胞因子和 I 型干擾素的產(chǎn)生Figure 1-3. Silencing of CaMKII expression attenuates TLR4,9,3-activatedproinflammatory cytokine and type I interferon production in macrophages.Mouse peritoneal macrophages (4 × 105) were transfected with control small RNA (Ctrl)or CaMKII-α siRNA1. After 48 hr, cells were stimulated with 0.1 μg/ml LPS (A), 0.3μM CpG ODN (B) or 10 μg/ml Poly(I:C) (C) for the indicated time. IL-6, TNF-α orIFN-β in the supernatants was measured by ELISA. Data are shown as mean ± SD ofthree independent experiments. **, P < 0.01.
CaMKII 能消除 CaMKII-α siRNA 對(duì) LP生的抑制α overexpression rescues CaMKII-α silenction in LPS-stimulated macrophages.d RAW264.7 cells were transfected withfter 36 hr, CaMKII-α and β-actin exprelot. Similar results were obtained in three inls (1.5 × 105) were transfected with contrAfter 36h, the cells were transfected withours later, the cells were stimulated with B) and IFN-β (C) in the supernatants wean ± SD of three independent experiments.
本文編號(hào)：3610756
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