MiR-155調(diào)控T細胞活化的機制研究
發(fā)布時間:2021-08-03 15:02
【研究背景和目的】:哮喘是嚴(yán)重危害人類健康的常見慢性呼吸道疾病之一,近年來其發(fā)病率呈逐年增加趨勢,目前尚無有效根治方法。近年來研究認(rèn)為:哮喘是一種復(fù)雜的異質(zhì)性疾病,其主要病理特征是氣道慢性炎癥,其發(fā)病的核心機制之一是在炎癥反應(yīng)過程中CD4+T淋巴細胞活化異常,Th2反應(yīng)增強,導(dǎo)致細胞因子失衡;但具體調(diào)控機理尚未完全闡明。Bic/miR-155基因敲除小鼠CD4+T細胞活化出現(xiàn)了異常,T細胞反應(yīng)明顯減弱;被破傷風(fēng)抗毒素(Tetc)免疫的該小鼠的脾臟細胞在體外Tetc刺激的過程中不能產(chǎn)生特異的IL-2和IFN-γ;且該小鼠在飼養(yǎng)320天之后出現(xiàn)了與哮喘患者類似的氣道重塑。這提示miR-155的缺失能夠造成細胞因子失衡并可能與哮喘的發(fā)病有關(guān)。然而Bic/miR-155基因敲除導(dǎo)致IL-2減少的作用機制尚未得到闡明。由于IL-2主要由T細胞在活化過程中產(chǎn)生,T細胞的活化需要TCR及共刺激分子雙信號的參與,我們認(rèn)為IL-2產(chǎn)生的減少可能是由于bic/ miR-155敲除的T細胞高表達了負向共刺激分子。BTLA和CTLA-4作為兩個非常重要的Ig超家族的...
【文章來源】:中國人民解放軍海軍軍醫(yī)大學(xué)上海市 211工程院校
【文章頁數(shù)】:71 頁
【學(xué)位級別】:博士
【部分圖文】:
TargetScan5.1(http://www.targetscan.org/)預(yù)測的miR-155與靶基因的3’-UTR結(jié)合區(qū)域
圖1:Target Scan 5.1(http://www.targetscan.org/)預(yù)測的miR-155 與靶基因的3’-UTR結(jié)合區(qū)域圖2: miRanda (http://www.microRNA.org) 預(yù)測的miR-155 與靶基因的3’-UTR結(jié)合區(qū)域相關(guān)博士學(xué)位論文 2011年 第09期 醫(yī)藥衛(wèi)生科技輯 E063-2-14
表 1 小鼠 BTLA3’-UTR 全長雙熒光素酶報告基因相關(guān)信息:Catalog No.: MmiT025047-MT01Gene Accession : NM_001037719.2 UTR Length: 2298 bpDescription: Mus muscμlus B and T lymphocyte associated (Btla), transcript variant 1, mRNAVector: pEZX-MT01 Vector Size: 7373 bp (backbone only, UTR insert not cAntibiotic: Kanamycin Stable Selection Marker : NeomycinReporter Genes: hLuc-hRluc Promoter : Sv405' Cutting Site: 3' Cutting Site :Suggested Sequencing PrimersForward: 5'-GATCCGCGAGATCCTGAT-3'Reverse: 5'-TTGGCGTTACTATGGGAACAT-3'
【參考文獻】:
期刊論文
[1]BTLA,a New Inhibitory B7 Family Receptor with a TNFR Family Ligand[J]. Chun Zeng~(1,2) Tinghe Wu~(1,2) Yu Zhen~(1,2) Xuepei Xia~3 Yong Zhao~(1,2,4) ~1Transplantation Biology Research Division,State Key Laboratory of Biomembrane and Membrane Biotechnology,Institute of Zoology,Chinese Academy of Sciences,Beijing 100080,China;~2Graduate School of Chinese Academy of Sciences,Beijing 100037,China;~3Department of Endocrinology,Beijing Haidian Hospital,Beijing 100080,China;~4Transplantation Biology Research Division,State Key Laboratory of Biomembrane and Membrane Biotechnology,Institute of Zoology,Chinese Academy of Sciences,25 Beisihuanxi Road,Haidian District,Beijing 100080,China.. Cellular & Molecular Immunology. 2005(06)
本文編號:3319833
【文章來源】:中國人民解放軍海軍軍醫(yī)大學(xué)上海市 211工程院校
【文章頁數(shù)】:71 頁
【學(xué)位級別】:博士
【部分圖文】:
TargetScan5.1(http://www.targetscan.org/)預(yù)測的miR-155與靶基因的3’-UTR結(jié)合區(qū)域
圖1:Target Scan 5.1(http://www.targetscan.org/)預(yù)測的miR-155 與靶基因的3’-UTR結(jié)合區(qū)域圖2: miRanda (http://www.microRNA.org) 預(yù)測的miR-155 與靶基因的3’-UTR結(jié)合區(qū)域相關(guān)博士學(xué)位論文 2011年 第09期 醫(yī)藥衛(wèi)生科技輯 E063-2-14
表 1 小鼠 BTLA3’-UTR 全長雙熒光素酶報告基因相關(guān)信息:Catalog No.: MmiT025047-MT01Gene Accession : NM_001037719.2 UTR Length: 2298 bpDescription: Mus muscμlus B and T lymphocyte associated (Btla), transcript variant 1, mRNAVector: pEZX-MT01 Vector Size: 7373 bp (backbone only, UTR insert not cAntibiotic: Kanamycin Stable Selection Marker : NeomycinReporter Genes: hLuc-hRluc Promoter : Sv405' Cutting Site: 3' Cutting Site :Suggested Sequencing PrimersForward: 5'-GATCCGCGAGATCCTGAT-3'Reverse: 5'-TTGGCGTTACTATGGGAACAT-3'
【參考文獻】:
期刊論文
[1]BTLA,a New Inhibitory B7 Family Receptor with a TNFR Family Ligand[J]. Chun Zeng~(1,2) Tinghe Wu~(1,2) Yu Zhen~(1,2) Xuepei Xia~3 Yong Zhao~(1,2,4) ~1Transplantation Biology Research Division,State Key Laboratory of Biomembrane and Membrane Biotechnology,Institute of Zoology,Chinese Academy of Sciences,Beijing 100080,China;~2Graduate School of Chinese Academy of Sciences,Beijing 100037,China;~3Department of Endocrinology,Beijing Haidian Hospital,Beijing 100080,China;~4Transplantation Biology Research Division,State Key Laboratory of Biomembrane and Membrane Biotechnology,Institute of Zoology,Chinese Academy of Sciences,25 Beisihuanxi Road,Haidian District,Beijing 100080,China.. Cellular & Molecular Immunology. 2005(06)
本文編號:3319833
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