【摘要】： 天然免疫反應(yīng)中TLR的激活可引起MAPKs和NF-kB的激活。信號調(diào)節(jié)蛋白SIRPα參與對MAPK和NF-kB信號通路的調(diào)節(jié)。SIRPα在LPS引起的天然免疫激活具有葦要的負性調(diào)節(jié)作用。LPS刺激后巨噬細胞SIRPα表達明顯下調(diào),這對于LPS誘導(dǎo)的初始天然免疫激活是必要的。干擾SIRPα后引起MAPKs和NF-kB信號通路的激活增強,一些前炎癥因了的釋放增多。尾靜脈輸入SIRPα干擾后的巨噬細胞的小鼠對LPS引起的內(nèi)毒素休克敏感性顯著增高,重要臟器的炎癥反應(yīng)明顯增強。SIRPα引起以上的負性調(diào)節(jié)作用可能主要通過抑制SHP-2和下游IKK家族蛋白結(jié)合發(fā)揮作用。
[Abstract]:Activation of TLR in innate immune response can induce activation of MAPKs and NF-kB. Signal regulatory protein SIRP 偽 involved in regulation of MAPK and NF-kB signaling pathway. SIRP 偽 down-regulated the expression of SIRP 偽 in macrophages induced by LPS. This is necessary for the initial innate immune activation induced by LPS. After interfering with SIRP 偽, the activation of MAPKs and NF-kB signaling pathway was enhanced, and some proinflammatory factors were increased. The sensitivity of macrophages induced by SIRP 偽 to endotoxic shock induced by LPS was significantly increased in mice injected into caudal vein. The inflammatory response of important organs is significantly enhanced. SIRP 偽 may play a role in inhibiting the binding of SHP-2 and downstream IKK family proteins.
【學(xué)位授予單位】：第二軍醫(yī)大學(xué)
【學(xué)位級別】：博士
【學(xué)位授予年份】：2007
【分類號】：R392

【共引文獻】

相關(guān)博士學(xué)位論文 前2條

1 康斌;SIRP α及Gankyrin在神經(jīng)發(fā)育和分化中的表達調(diào)控和作用研究[D];第二軍醫(yī)大學(xué);2004年

2 劉瓊;信號調(diào)節(jié)蛋白α在樹突狀細胞活化中的調(diào)節(jié)作用和射頻消融術(shù)聯(lián)合熱休克DC疫苗抑制腫瘤復(fù)發(fā)[D];第二軍醫(yī)大學(xué);2009年

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