钙/钙调素依赖性蛋白激酶Ⅱ和MHC Ⅱ类分子对TLR触发的巨噬细胞与树突状细胞天然免疫应答反应的调控及其机制研究
发布时间：2022-01-26 15:50
Toll样受体（Toll-like receptors, TLRs）作为一类重要的模式识别受体（Pattern recognition receptors, PRRs）主要表达于巨噬细胞和树突状细胞（Dendritic cells, DCs）表面,选择性地识别病原体相关分子模式（Pathogen-associated molecular patterns, PAMPs）,构成机体免疫系统抵御病原体入侵的第一道屏障。TLR是一类在各种生物体内高度保守的I型跨膜蛋白,目前已在哺乳动物中发现并克隆了12种。一旦识别了病原体中特定的分子结构,TLR就会激活其下游一系列的信号通路,活化天然免疫细胞产生炎性细胞因子和I型干扰素。TLR不仅启动天然免疫应答,控制炎症反应的性质、强度和持续时间,还可以通过上调DC表面的MHC II类分子和共刺激分子,促进DC的成熟,指导抗原特异的免疫应答尤其是Th1型反应的产生,调节获得性免疫应答的强度和类型,成为连接初始免疫应答和获得性免疫应答的桥梁。TLR信号过度活化或活化不足会导致机体功能异常和疾病的发生。许多的其他信号通路参与对TLR信号的严密调控。因此,对T...
【文章来源】：中国人民解放军海军军医大学上海市 211工程院校
【文章页数】：111 页
【学位级别】：博士
【部分图文】：
干扰RAW264.7细胞中CaMKII的表达能抑制LPS触发的炎性细胞因子和I型干扰素的产生Figure1-2.SilencingofCaMKIIexpressionattenuatesTLR4-activatedproinflammatorycytokineandtypeIinterferonproductioninRAW264.7cells.
图 1-3. 干扰小鼠腹腔巨噬细胞中 CaMKII 的表达能抑制 TLR3、4、9 促发的炎性细胞因子和 I 型干扰素的产生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 对 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.
本文编号：3610756
【文章来源】：中国人民解放军海军军医大学上海市 211工程院校
【文章页数】：111 页
【学位级别】：博士
【部分图文】：
干扰RAW264.7细胞中CaMKII的表达能抑制LPS触发的炎性细胞因子和I型干扰素的产生Figure1-2.SilencingofCaMKIIexpressionattenuatesTLR4-activatedproinflammatorycytokineandtypeIinterferonproductioninRAW264.7cells.
图 1-3. 干扰小鼠腹腔巨噬细胞中 CaMKII 的表达能抑制 TLR3、4、9 促发的炎性细胞因子和 I 型干扰素的产生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 对 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.
本文编号：3610756
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