本文選題：血管活性腸肽　切入點(diǎn)：樹突狀細(xì)胞　出處：《浙江大學(xué)》2006年碩士論文　論文類型：學(xué)位論文

【摘要】：樹突狀細(xì)胞(DC)是體內(nèi)抗原提呈功能最強(qiáng)的抗原提呈細(xì)胞(APC),在誘導(dǎo)免疫應(yīng)答中起著非常關(guān)鍵的作用。DC表達(dá)高水平的MHC分子、共刺激分子、粘附分子和Th1型細(xì)胞因子等,是已知唯一能活化初始T、B細(xì)胞的抗原提呈細(xì)胞。骨髓來源的DC前體細(xì)胞通過血流幾乎能到達(dá)所有的組織,成為定居的未成熟DC(iDC),監(jiān)視外來的抗原。當(dāng)捕獲抗原后,DC通過輸入淋巴管從外周組織遷移到二級淋巴器官,啟動特異性免疫應(yīng)答。在遷移過程中,iDC經(jīng)歷表型和功能成熟,尤其是DC表面趨化因子受體的表達(dá)及對不同趨化因子的趨化活性改變,與DC的成熟階段和功能活化緊密相關(guān)。iDC表達(dá)許多炎癥性趨化因子受體,如CCR1、CCR2、CCR5和CCR6,能與許多CC和CXC趨化因子結(jié)合,如MIP-1α、MIP-1β、RANTES和MIP-3α,有利于iDC向炎癥部位聚集。當(dāng)DC成熟時,炎癥性趨化因子受體表達(dá)下調(diào)或活性減低,對這些趨化因子中的大多數(shù)失去了應(yīng)答能力,同時上調(diào)趨化因子受體CCR7的表達(dá),其配體為表達(dá)于次級淋巴組織的MIP-3β和6Ckine,這些因素促使成熟DC(mDC)離開炎癥部位,向淋巴組織遷移完成抗原提呈功能。有研究表明,CCR1和CCR5及其配體在iDC遷移到炎癥部位中起著重要的作用;而CCR7與MIP-3β的相互作用則是mDC
[Abstract]:Dendritic cell (DC) is the most potent antigen presenting cell in vivo, which plays a key role in inducing immune response. DC expresses high level of MHC molecules, costimulatory molecules, adhesion molecules and Th1 type cytokines. Is the only antigen presenting cell known to activate the initial TGB cells. DC progenitor cells derived from bone marrow can reach almost all tissues through blood flow. When the antigen is captured, the DC migrates from the peripheral tissue to the secondary lymphoid organ, and initiates a specific immune response. During the migration, the DC experiences phenotypic and functional maturation. In particular, the expression of chemokine receptors and the changes of chemokine activity on the surface of DCs are closely related to the mature stage and functional activation of DC. IDC expresses many inflammatory chemokine receptors. For example, CCR1, CCR2, CCR5 and CCR6 can bind to many CC and CXC chemokines, such as MIP-1 偽 -MIP-1 尾 -RANTES and MIP-3 偽, which is conducive to the aggregation of iDC to the inflammatory site. When DC matures, the expression of inflammatory chemokine receptors is down-regulated or the activity decreases. Most of these chemokines lost their ability to respond, and up-regulated the expression of chemokine receptor CCR7, the ligand of which were MIP-3 尾 and 6Ckinein expressed in secondary lymphoid tissues, which caused the mature DCM to leave the inflammatory site. Migration to lymphoid tissues completes antigen presentation. Studies have shown that CCR1, CCR5 and their ligands play an important role in the migration of iDC to the inflammatory site, while the interaction between CCR7 and MIP-3 尾 is mDC.
【學(xué)位授予單位】：浙江大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2006
【分類號】：R392

【參考文獻(xiàn)】

相關(guān)期刊論文 前1條

1 徐海燕;血管活性腸肽的免疫調(diào)節(jié)作用[J];國外醫(yī)學(xué)(免疫學(xué)分冊);2002年02期

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本文編號：1601419