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| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 李建國(Chien-Kuo Lee) | |
| dc.contributor.author | Yan Zeng | en |
| dc.contributor.author | 曾妍 | zh_TW |
| dc.date.accessioned | 2022-11-24T03:05:34Z | - |
| dc.date.available | 2021-05-04 | |
| dc.date.available | 2022-11-24T03:05:34Z | - |
| dc.date.copyright | 2021-05-04 | |
| dc.date.issued | 2021 | |
| dc.date.submitted | 2021-04-27 | |
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| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/80385 | - |
| dc.description.abstract | "樹突狀細胞（DC）包括傳統樹突細胞（conventional DCs , cDC）和槳狀樹突細胞（plasmacytoid DCs , pDC），這兩種細胞在先天和適應性免疫中扮演重要角色。我們先前發現類鐸受體（Toll like receptor, TLR）誘導的發炎反應會減少pDC的發育，但會增加cDC的產生。然而，由發炎反應誘導出的DC的功能仍不清楚。在我們的研究中證實在DC發育過程中接受了TLR7信號會削弱分化出的DC的活化和功能，這包括表現在細胞表面的活化標誌物比如CD40，PD-L1，CD86，MHCII等訊號在pDC和cDC中的表現量均顯著降低。DCs也產生較少的發炎細胞素，例如IL-6，IL-12和TNF-α在RNA和蛋白質的量都減少，然而，IL-10（一種抑制發炎細胞素）則略有增加。此外，用DQ-OVA熒光裂解的方式測試抗原分解能力的實驗中，發現這種能力也被抑制，這些結果顯示發炎反應所誘導的DC具有更大的耐受引發能力。此外，DC發育中的TLR7信號傳導也會降低粒線體膜電位和質量。與對照組相比，事先用R848處理的DC中的粒線體的ROS降低了。這些結果顯示，代謝能力變差有可能與DC功能受損有關。為了研究R848如何改變DC活化及功能，我們使用了STAT3，AKT，mTOR和p38的抑制劑，我們發現mTOR抑製劑（Rapamycin）可部分恢復發炎反應所誘導的DCs活化標誌的表現。p38抑制劑（SB203580）則可以通過上調活化標記和促炎細胞素的產生，明顯逆轉了R848所改變的DC的活化。此外，p38抑制劑也逆轉了TLR7所介導的粒線體ROS，粒線體膜電位和質量的降低。因此，在我們的研究中，已經證明在DC發育過程中TLR7訊號通過活化p38去造成所分化出的DCs的功能的嚴重損害，粒線體動力學和ROS。這些結果或許可以解釋慢性發炎造成的免疫缺陷，並提供治療慢性發炎或自體免疫疾病（例如，發炎性腸炎（Inflammatory bowel disease, IBD）及類風濕性關節炎）的治療方法。" | zh_TW |
| dc.description.provenance | Made available in DSpace on 2022-11-24T03:05:34Z (GMT). No. of bitstreams: 1 U0001-1804202119275600.pdf: 7350319 bytes, checksum: 94cf48eee95877f6ece13dce8744d8c7 (MD5) Previous issue date: 2021 | en |
| dc.description.tableofcontents | "致謝----------------------------------------------------------------------i 中文摘要-------------------------------------------------------------------ii Abstract------------------------------------------------------------------iii Abbreviations-------------------------------------------------------------v Content-------------------------------------------------------------------vi Chapter I Introduction----------------------------------------------------1 1.1 Dendritic cell subset---2 1.2 Dendritic cell development---4 1.3 Hematopoiesis during inflammation---5 1.4 Metabolism is an essential of Immune function modulator---6 1.5 PI3K-AKT-mTOR signaling pathway---7 1.6 P38-MAPK signaling pathway---8 1.7 Rationale and specific aims---9 Chapter II Materials and Methods---10 2.1 Mice---11 2.2 Generation and cell culture of Hoxb8-FL progenitor cell line---11 2.3 Cell sorting---11 2.4 In vitro culture and differentiation of iHSPC with R848 treatment---12 2.5 In vitro culture and differentiation of primary progenitors with R848 treatment---12 2.6 Flow cytometry---13 2.7 Antigen Processing Study---13 2.8 Quantitative real-time PCR---13 2.9 Enzyme-linked immunosorbent assay (ELISA)---14 2.10 Mitochondrial Ros---14 2.11 Mitochondrial membrane potential and mass---14 2.12 Intracellular staining---15 2.13 Immunobloting---15 2.14 Statistical analysis---16 2.15 Formula of reagents---16 Table 1. The list of antibodies---16 Chapter III Results---------------------------------------------------------18 3.1 The effects of TLR7 signaling on reprograming the development and activation of DCs.---19 3.2 TLR7 signaling during DC development impairs the antigen processing ability of cDC.---20 3.3 TLR7 signaling during DC development impairs CpG-stimulated cytokine production from DCs---21 3.4 TLR7 signaling during DC development does not affect TLR9-signaling activation in DCs---22 3.5 WP1066, a STAT3 inhibitor, partially blocks TLR7 signaling-mediated inhibition of DC---22 3.6 mTOR inhibitor partially blocks TLR7 signaling-mediated inhibition of DC activation---23 3.7 SB203580, a p38 inhibitor, blocks TLR7-signaling mediated effects on DC development, activation and cytokine production---24 3.8 TLR7 signaling during DC development alters mitochondrial dynamics---26 3.9 SB203580, a p38 inhibitor blocks TLR7-signaling mediated downregulation of mitochondrial dynamics in DCs---28 Conclusion remarks 29 Chapter IV Discussion 30 4.1 Reprogramming of dendritic cell in presence of TLR7 stimulation---31 4.2 The STAT3/AKT/mTOR pathways are involved in reprogramming of DC development and activation by TLR7 signaling.---33 4.3 The p38 MAPK pathway are essential for reprogramming of dendritic cell development, activation and function by TLR7 signaling.---34 Chapter V References------------------------------------------------------36 Chapter VI Figures----------------------------------------------------------41 Figure 1. TLR7 signaling reprograms DC development and suppresses activation ability of the DCs.---44 Figure 2. TLR7 signaling reprograms DC development and suppresses the activation of BM-derived DCs---49 Figure 3. TLR7 signaling reprograms DC development and suppresses the activation of Lin- Flt3+-derived DCs.---54 Figure 4. TLR7 signaling during DC development impairs the antigen processing ability of cDC.---57 Figure 5. TLR7 signaling during DC development impairs CpG-stimulated cytokine production from DCs.---59 Figure 6. TLR7 signaling during DC development does not affect TLR9-signaling activation in DCs---60 Figure 7. WP1066, a STAT3 inhibitor, partially blocks TLR7 signaling-mediated inhibition of DC.---62 Figure 8. Ly294002, a AKT inhibitor, have no effects on TLR7 signaling-mediated inhibition of DC.---64 Figure 9. Rapamycin, a mTOR inhibitor, partially blocks TLR7 signaling-mediated inhibition of DC activation.---66 Figure 10. SB203580, p38i inhibitor, induced TLR7-signaling mediated DC development and activation.---69 Figure 11. p38i blocks TLR7 signaling mediated inhibition of CpG-stimulated cytokine production by DCs.---71 Figure 12. TLR7 signaling during DC development affects mitochondrial dynamics Figure 13. TLR7 signaling during DC development impairs Mitochondrial membrane potential---77 Figure 14. TLR7 signaling during DC development impairs Mitochondrial mass ---80 Figure 15. TLR7 signaling during DC development impairs Mitochondrial ROS production in DCs.---82 Figure 16. p38i blocks TLR7-signaling-induced downregulation of MDR/MG in DCs. 85 Figure 17. p38i blocks TLR7 signaling-mediated inhibition of mitochondrial ROS production in DCs.---87 " | |
| dc.language.iso | zh-TW | |
| dc.subject | 絲裂原活化蛋白激酶 | zh_TW |
| dc.subject | 類鐸受體 | zh_TW |
| dc.subject | 樹突細胞 | zh_TW |
| dc.subject | 發炎 | zh_TW |
| dc.subject | p38 | en |
| dc.subject | inflammation | en |
| dc.subject | Dendritic cell | en |
| dc.subject | Toll like receptor | en |
| dc.title | 發育過程中的第七型類鐸受體訊號抑制樹突細胞的活化和功能 | zh_TW |
| dc.title | TLR7 signaling during dendritic cell development suppresses their activation and function | en |
| dc.date.schoolyear | 109-2 | |
| dc.description.degree | 碩士 | |
| dc.contributor.oralexamcommittee | 徐立中(Hsin-Tsai Liu),嚴仲陽(Chih-Yang Tseng) | |
| dc.subject.keyword | 類鐸受體,樹突細胞,發炎,絲裂原活化蛋白激酶, | zh_TW |
| dc.subject.keyword | Toll like receptor,Dendritic cell,inflammation,p38, | en |
| dc.relation.page | 87 | |
| dc.identifier.doi | 10.6342/NTU202100835 | |
| dc.rights.note | 同意授權(限校園內公開) | |
| dc.date.accepted | 2021-04-28 | |
| dc.contributor.author-college | 醫學院 | zh_TW |
| dc.contributor.author-dept | 免疫學研究所 | zh_TW |
| 顯示於系所單位： | 免疫學研究所 | |
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