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研究生:徐翠玲
研究生(外文):Tsui-Ling Hsu
論文名稱:第三號誘餌受體的功能鑑定
論文名稱(外文):Functional Characterization of Decoy Receptor 3
指導教授:謝世良
指導教授(外文):Shie-Liang Hsieh
學位類別:博士
校院名稱:國立陽明大學
系所名稱:微生物及免疫學研究所
學門:生命科學學門
學類:微生物學類
論文種類:學術論文
論文出版年:2004
畢業學年度:92
語文別:英文
論文頁數:128
中文關鍵詞:第三號誘餌受體腫瘤壞死因子
外文關鍵詞:Decoy Receptor 3Tumor Necrosis Factor
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第三號誘餌受體 (decoy receptor 3) 為腫瘤壞死因子受體家族中的一員,它可藉由與其配體的結合而中和FasL或LIGHT造成的細胞毒性、降低LIGHT或TL1A激活T細胞的能力、並阻斷TL1A的生物功能而促進血管新生,因此被認為是一具有免疫抑制能力的分子。由於文獻報導在癌病組織中可發現功能不全的樹狀細胞,而在多種癌症病人的病理組織及血清中皆可偵測到第三號誘餌受體,我們於是開始探討第三號誘餌受體對樹狀細胞的免疫調控能力。我們的研究結果發現第三號誘餌受體可以影響樹狀細胞的分化及活化,其中包含調節細胞表面抗原及細胞激素的表現量:樹狀細胞上的表面抗原CD86/B7.2表現量上升,而CD40、CD54/ICAM-1、CD80/B7.1、CD1a及HLA-DR的表現量則會下降;成熟樹狀細胞分泌IL-10及IL-12能力則被抑制。被第三號誘餌受體處理過的樹狀細胞促進CD4+ T細胞增生的能力明顯地減弱,在我們的實驗中更發現其顯著地激活了CD4+ T細胞產生較高量的IL-4、IL-5及IL-10。這些結果暗示腫瘤細胞可藉著分泌第三號誘餌受體,而引導免疫系統產生較不利於清除腫瘤的第二型輔助T細胞免疫反應,因此達到逃避免疫系統攻擊的目的。為了更明暸第三號誘餌受體在體內的功能,我們將它表現於基因轉殖小鼠並研究其功能,發現第三號誘餌受體的表達可以有效地抑制Fas/FasL所引起的活化引發死亡機制 (activation-induced cell death),但無法產生與Fas缺陷小鼠 (lpr/lpr) 相同的淋巴球增生現象。表現第三號誘餌受體的小鼠脾臟細胞在受刺激後產生較高量的IL-4和IL-10,並有IFN-γ、IL-12及TNF-α 表現量減少的情形。進一步的實驗結果顯示,被Listeria monocytogenes感染的第三號誘餌受體基因轉殖小鼠產生IFN-γ 的能力明顯降低,同樣地,牠們也較無法產生對抗感染的免疫能力而有較高的死亡率。結果顯示,第三號誘餌受體同樣地在體內引起了偏向第二型輔助T細胞的免疫反應,而其引發此現象的機制則須要更進一步的探究。
The soluble decoy receptor 3 (DcR3) is a member of the tumor necrosis factor receptor (TNFR) superfamily. DcR3 is able to modulate host response via neutralizing the biological effects of Fas ligand (FasL), LIGHT and TL1A. In addition, it has been demonstrated that DcR3 is up-regulated in various cancers, therefore DcR3 is regarded as an immuno-suppressor to down-regulate immune responses. We found that DcR3.Fc profoundly modulated dendritic cells (DCs) differentiation and maturation from CD14+ monocytes, including the up-regulation of CD86/B7.2, and the down-regulation of CD40, CD54/ICAM-1, CD80/B7.1, CD1a, and HLA-DR, as well as the attenuation of interleukin (IL)-10 and IL-12 secretion. Moreover, DcR3.Fc-treated DCs suppressed CD4+ T cell proliferation in an allogeneic mixed lymphocyte reaction (MLR) and up-regulated IL-4, IL-5 and IL-10 secretion of CD4+CD45RA+ T cells. This suggests that DcR3 may not only act as a decoy receptor to FasL, LIGHT and TL1A, but also act as an effective molecule to skew T cell response to Th2 phenotype. To further address the functions of DcR3 in vivo, transgenic mice over-expressing DcR3 were generated. It is interesting to note that FasL-dependent cell apoptosis is inhibited in DcR3 transgenic mice, but the size of spleen and lymph nodes were not enlarged as those of lpr/lpr mice. Moreover, the secretion of IL-4 and IL-10 is up-regulated, whilst the secretion of IFN-γ, IL-12 and TNF-α is down-regulated in the HA126-138 peptide-stimulated splenocytes of HNT-DcR3 double transgenic mice. When infected with Listeria monocytogenes, DcR3 transgenic mice showed lower expression of IFN-γ and higher susceptibility to infection. These data confirmed the roles of DcR3 to attenuate Th1 response, and indicated that DcR3 might be one of the immuno-suppressor secreted by tumor cells to help tumor invasion.
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