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完整後設資料紀錄
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.advisor | 朱清良(Ching-Liang Chu) | |
dc.contributor.author | Yi-Gen Pan | en |
dc.contributor.author | 潘毅耕 | zh_TW |
dc.date.accessioned | 2021-06-17T03:45:46Z | - |
dc.date.available | 2023-02-22 | |
dc.date.copyright | 2018-02-22 | |
dc.date.issued | 2018 | |
dc.date.submitted | 2018-01-30 | |
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dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/70141 | - |
dc.description.abstract | 痛風是因尿酸結晶(monosodium urate)沉積在組織所引起的發炎疾病。沉積的結晶使巨噬細胞(macrophage)NLRP3炎性體(Inflammasome)活化產生第一型介白素貝塔(IL-1ß)並使嗜中性白血球(Neutrophil)生聚集型嗜中性白血球胞外網狀結構(aggregated neutrophil extracellular traps, aggregated NETs)導致紅腫疼痛和組織傷害。研究指出第三號誘餌受體(decoy receptor 3, DcR3)可抑制脂多糖(lipopolysaccharide, LPS)及病毒所造成之發炎反應。然而第三號誘餌受體對於尿酸結晶在巨噬細胞引起的NLRP3炎性體的反應尚未被探討。在此我們發現第三號誘餌受體藉由其硫酸乙醯肝素(Haparan sulfate)結合位點抑制結晶在巨噬細胞上引起的第一型介白素貝塔產生以及NLRP3炎性體活化。第三號誘餌受體可能藉由抑制溶小體(Lysosome)裂解和粒線體(Mitochondria)活性氧化物質(ROS)產生來達到抑制NLRP3炎性體的活化。第三號誘餌受體可能藉由抑制的F型和K型組織蛋白酶(Cathepsin)表現使溶小體較穩定並抑制裂解。此外第三號誘餌受體轉殖鼠在受到尿酸結晶刺激時也產生較少的第一型介白素貝塔和趨化因子(Chemokines)且免疫細胞浸潤較緩和。結合以上結果我們得知第三號誘餌受體可減緩尿酸引起的發炎並治療痛風。此外之前研究表示第三號誘餌受體和抗體抗原結晶區(Fc region)的複合蛋白的功能需藉由其抗體抗原結晶區而抗體受體的信號傳遞轉接蛋白(FcƐR I- Ƴ chain, FcRƳ)在特定情況下可傳遞抑制訊號去調控其他受體。在此我們將探討信號傳遞轉接蛋白如何調控擁有與其類似訊號傳遞的表面受體Dectin-1的反應。我們發現Fcer1g-/-樹突細胞中受到Dectin-1刺激後產生較多細胞激素且細胞較成熟並可活化較多的Th17輔助細胞。進一步的分析中我們也發現在Fcer1g-/-樹突細胞中Dectin-1的訊號也較強。增強的訊號可能是樹突細胞Dectin-1受到刺激時,FcRƳ與磷酸酶(phosphatase);SHP-1和PTEN結合並抑制Dectin-1訊號。由於Dectin-1對於抗真菌和癌症細胞及佐劑免疫反應扮演很重要的腳色,因此我們的研究成果將可以應用到疫苗開發以及癌症治療的應用。 | zh_TW |
dc.description.abstract | Gout is a common inflammatory arthritis caused by deposition of monosodium urate (MSU) crystal in joint. The shedding MSU crystals lead locally inflammatory responses including NLRP3-dependent IL-1ß secretion and immune cells infiltration. Previously, we showed that DcR3.Fc suppresses LPS- and virus-induced inflammatory responses in macrophage. In this study, we found that crystals-induced IL-1ß secretion and NLRP3 activation were suppressed by both DcR3.Fc and HBD.Fc. Suppression of MSU-induced NLRP3 inflammsome activation through inhibition of lysosome rupture and mitochondria ROS production by DcR3. Agree with in vitro results, MSU-induced less amount of IL-1ß and chemokines secretion and neutrophil recruitment in DcR3-tg. Thus, DcR3 may have potential application for gout treatment. Because some DcR3-mediated effects are based on Fc region and FcɛRIƳ-chain (FcRƳ), which is an ITAM-containing adaptor protein of Fc receptor can deliver negative signaling to modulate responses of other receptors. Thus, we wanted to investigate the inhibitory mechanism of ITAM-containing adaptors. We found that the responses of Dectin-1 containing own hemITAM motif were enhanced in FcRƳ-deficient but not DAP12-deficient dendritic cells (DCs). This strengthen Dectin-1 responses were not observed in FcRƳ-deficient macrophage. Agree with the augmented Dectin-1 responses in FcRƳ-deficient DCs, Dectin-1-mediated Th17 polarizations were also enhanced in FcRƳ-deficient DCs. Furthermore, we discovered that FcRƳ-deficient DCs had stronger Dectin-1 signaling than WT mice. The enhanced Dectin-1 signaling may be resulted from phosphatases SHP-1and PTEN which were recruited to FcRƳ and negatively modulated Dectin-1 activation. Thus, our findings provide a novel mechanism for Dectin-1 responses modulation by FcRƳ and this novel modulation mechanism of Dectin-1 can be applied to vaccine preparation and cancer therapy. | en |
dc.description.provenance | Made available in DSpace on 2021-06-17T03:45:46Z (GMT). No. of bitstreams: 1 ntu-107-D00449005-1.pdf: 7966849 bytes, checksum: eed2dd0892990f78bde8ccabead9cdc5 (MD5) Previous issue date: 2018 | en |
dc.description.tableofcontents | 謝誌 I
摘要 III Abstract IV Contents V I. Introduction 1 I.1. Molecular Mechanism of DcR3-mediated Suppression on Crystal-induced Inflammation 1 I.1.1. Tumor Necrosis Factor Superfamily (TNFSF) and TNF Receptor (TNFR) .........................................................................................................................1 I.1.2. Decoy receptor 3 (DcR3) 2 I.1.3. Gout 4 I.1.4. Macrophage 5 I.1.5. Neutrophil 7 I.1.6. NLRP3 Inflammasome 8 I.1.7. Cystein Cathepsin Proteases 9 I.2. FcγRI gamma-chain negatively modulates Dectin-1 Responses in dendritic cells. ................................................................................................................................10 I.2.1. Innate Immune System 11 I.2.2. Dendritic Cell (DC) 12 I.2.3. C-type lectin receptors (CLRs) 12 I.2.4. Imuunoreceptor Tyrosin-based Activation Motif (ITAM)–containing Adaptors .......................................................................................................................15 I.2.5. ITAM- and ITIM-associated Phosphatases 17 II. Specific Aims 22 II.1. Molecular Mechanism of DcR3-mediated Suppression on Crystal-induced Inflammation 22 II.2. FcγRI gamma-chain Negatively Modulates Dectin-1 Responses in Dendritic Cells. ................................................................................................................................23 III. Materials and Methods 26 III.1. Molecular Mechanism of DcR3-mediated Suppression on Crystal-induced Inflammation 26 III.1.1. Mice and Reagents 26 III.1.2. Preparation of MSU 26 III.1.3. Production of Recombinant DcR3.Fc and HBD,Fc Fusion Proteins 26 III.1.4. Macrophage Cultures 27 III.1.5. Cytokines Assays 27 III.1.6. Flow Cytometry Assays 28 III.1.7. Confocal Microscopy 28 III.1.8. Real-time PCR 29 III.1.9. Induction of AggNETs 29 III.1.10. Air Pouch Model 30 III.1.11. Histologic Analysis 30 III.1.12. Statistic 31 III.2. FcɛRI gamma-chain Negatively Modulates Dectin-1 Responses in Dendritic Cells. ................................................................................................................................31 III.2.1. Mice and DC/Macrophage Cultures 31 III.2.2. DC/Macrophage Maturation and Cytokines Production 32 III.2.3. Migration of DCs 32 III.2.4. Real-time PCR 33 III.2.5. Antigen-specific T cell responses 33 III.2.6. Western Blot 34 III.2.7. Immunopriciptation 35 III.2.8. Statistics 35 IV. Results 36 IV.1. Molecular Mechanism of DcR3-mediated Suppression on Crystal-induced Inflammation 36 IV.1.1. Suppression of IL-1ß Secretion in MSU-stimulated Macrophages by DcR3.Fc .......................................................................................................................36 IV.1.2. HBD Domain of DcR3 Mediated the Suppression of Particles-induced IL-1ß Secretion in Macrophages 37 IV.1.3. DcR3.Fc did not Suppress LPS-induced NLRP3 Components Induction in Macrophages 37 IV.1.4. MSU-induced Activation of NLRP3 Inflammasome was Impaired in DcR3.Fc-treated Macrophages 38 IV.1.5. MSU Engulfment was Regular in DcR3.Fc-treated Macrophages 38 IV.1.6. Suppression of MSU-induced Lysosome Rupture in Macrophages by DcR3 .......................................................................................................................39 IV.1.7. Expression of Cysteine Cathepsin F and K, but not Cathepsin B were suppressed in Macrophage by DcR3 39 IV.1.8. Suppression of MSU-induced Mitochondrial ROS Production in Macrophages by DcR3 40 IV.1.9. Suppression of MSU-induced AggNETs Formation in Neutrophil by DcR3 .......................................................................................................................41 IV.1.10. Low Amount of MSU-induced Inflammatory Cytokines were Induced by MSU in DcR3-transgenic Mice 41 IV.1.11. Low Amount of Infiltrating Immune Cells were Recruited after MSU Treatment in DcR3-tg 42 IV.1.12. Low Amount of MSU-induced Inflammatory Cytokines were Induced by MSU in DcR3.Fc-treate Mice 42 IV.1.13. Most of Infiltrating Cells were CD206+ Arg 1+ in MSU-treated DcR-tg Mice .......................................................................................................................43 IV.2. FcɛRI gamma-chain Negatively Modulates Dectin-1 Responses in Dendritic Cells ................................................................................................................................44 IV.2.1. Augmentation of Dectin-1-mediated Maturation in Fcer1g-/- and Tyrobp-/-Fcer1g-/- DCs, but not Tyrobp-/- DCs 44 IV.2.2. Augmentation of Dectin-1-mediated Cytokines Production in Fcer1g-/- and Tyrobp-/-Fcer1g-/- DCs, but not Tyrobp-/- DCs. 45 IV.2.3. Augmented-Dectin-1 Responses in Fcer1g-/- DCs were not Due to Different Cell Surface Level of Dectin-1. 45 IV.2.4. Augmented-Dectin-1 Responses in Fcer1g-/- DCs were not Due to Different Property of DC. 46 IV.2.5. Augmented-Dectin-1 Responses in Fcer1g-/- DCs were not a Ligand-specific Effect. 46 IV.2.6. Lack FcRƳ also enhanced Dectin-1- and TLR4-induced Anti-inflammatory Responses in DCs. 47 IV.2.7. FcRƳ did not influence Dectin-1 and TLR4 Responses in Macrophage. 47 IV.2.8. FcRƳ was not involved in Dectin-1 Ligands-induced Migration in DCs. 47 IV.2.9. OVA-specific T Cell Proliferation and Differentiation were enhanced in Fcer1g-/- BMDCs. 48 IV.2.10. OVA-specific T Cell Proliferation and Differentiation were Enhanced in Fcer1g-/- BMDCs. 49 IV.2.11. Dectin-1 Signaling was Strengthen in Fcer1g-/- DCs. 49 IV.2.12. Recruitment of Phosphatase, SHP-1 and PTEN, by FcRƳ after Dectin-1 Activation. 50 IV.2.13. SHP-1 and PTEN Modulate Dectin-1 Responses Negatively. 51 V. Discussions 52 V.1. Molecular Mechanism of DcR3-mediated Suppression on Crystal-induced Inflammation 52 V.2. FcɛRI gamma-chain Negatively Modulates Dectin-1 Responses in Dendritic Cells ................................................................................................................................54 VI. References 58 VII. Figures 70 IV. Appendix 96 | |
dc.language.iso | en | |
dc.title | 探討DcR3和FcƐRI gamma-chain調控先天免疫反應之機制 | zh_TW |
dc.title | Modulation of innate immune responses by DcR3 and FcƐRI gamma-chain | en |
dc.type | Thesis | |
dc.date.schoolyear | 106-1 | |
dc.description.degree | 博士 | |
dc.contributor.coadvisor | 謝世良(Shie-Liang Hsieh) | |
dc.contributor.oralexamcommittee | 賴明宗(Ming-Zong Lai),林琬琬(Wan-Wan Lin),陳俊任(Chun-Jen Chen),徐嘉琳(Chia-Lin Hsu) | |
dc.subject.keyword | 樹突細胞,巨噬細胞,免疫調控, | zh_TW |
dc.subject.keyword | Dendritic cell,macrophage,DcR3,FcRgamma, | en |
dc.relation.page | 96 | |
dc.identifier.doi | 10.6342/NTU201800235 | |
dc.rights.note | 有償授權 | |
dc.date.accepted | 2018-01-31 | |
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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