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| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 江伯倫 | zh_TW |
| dc.contributor.advisor | Bor-Luen Chiang | en |
| dc.contributor.author | 李宗翰 | zh_TW |
| dc.contributor.author | Tsung-Han Lee | en |
| dc.date.accessioned | 2024-08-16T17:41:07Z | - |
| dc.date.available | 2024-08-17 | - |
| dc.date.copyright | 2024-08-16 | - |
| dc.date.issued | 2024 | - |
| dc.date.submitted | 2024-08-07 | - |
| dc.identifier.citation | 1. Jackson, D.J., et al., IL-33-dependent type 2 inflammation during rhinovirus-induced asthma exacerbations in vivo. Am J Respir Crit Care Med, 2014. 190(12): p. 1373-82.
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| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/94715 | - |
| dc.description.abstract | 氣喘是一種由異常的第二型免疫反應引起的呼吸系統過敏性疾病。在氣喘發作時，過敏原或化學毒性分子等會破壞並誘導氣道上皮細胞釋放危險信號。這些元素還可以被固有層中的樹突狀細胞吸收，並促進輔助型T細胞2型（Th2）的生成。除此之外，組織駐留的第二型固有淋巴細胞（ILC2）也可以被危險信號激活，並釋放第二型細胞激素以招募嗜酸性粒細胞、產生黏液和促進平滑肌收縮。皮質類固醇是一種強效的糖皮質激素受體激動劑，用於抗發炎以抑制氣喘發作。儘管如此，這些藥物在臨床治療中會引發強烈的副作用。先前的研究表明，皮質類固醇可以誘導T細胞的凋亡。然而，皮質類固醇誘導的不同免疫細胞亞群的凋亡機制尚未被探討。在此，我們闡明了Dexamethasone調節第二型免疫反應相關風險的機制。首先，我們證明了Dexamethasone可以抑制Th1和Th2細胞中第一型和第二型細胞因子的產生。另外，我們發現，與Th1和Th0細胞相比，Th2細胞可以通過上調Bcl-2抗凋亡基因表達來抵抗Dexamethasone誘導的細胞凋亡現象以啟動抗凋亡反應。另一方面，ILC2仍然是第二型免疫反應中的關鍵淋巴細胞，我們檢測了小鼠肺部中的ILC和ILC2群體，發現ILC2是小鼠肺部中主要的ILC亞群。除此之外，不同性別的小鼠肺部組織駐留的ILC和ILC2也表現出不同的群體分佈。最終，我們發現Dexamethasone可抑制ILC2的二型細胞激素分泌能力，但並未在ILC2中誘導出明顯的凋亡現象。總而言之，第二型免疫細胞對Dexamethasone誘導的細胞凋亡具有抗性，這一現象表明Dexamethasone可能會影響第一型和第二型免疫之間的平衡。 | zh_TW |
| dc.description.abstract | Asthma is an allergic disease caused by abnormal type two immunity in the respiratory system. During the asthma attack, the allergen or chemical toxin sabotages and induces the release of danger signals by airway epithelial cells. These elements can also be taken up by dendritic cells in the lamina propria and promote the generation of T-helper 2 cells (Th2). In addition, tissue-resident type 2 innate lymphoid cells (ILC2) can be activated by danger signals and release type two cytokines for eosinophil recruitment, mucus production, and smooth muscle contraction. Corticosteroids are strong glucocorticoid receptor agonists used for anti-inflammatory purposes to suppress asthma attacks. Still, these medications trigger strong side effects during clinical treatment. Previous studies show that corticosteroids can induce the apoptotic phenomenon in T cells. However, the mechanism of the corticosteroid-induced apoptotic phenomenon in different immune cell subsets remains unexplored. Here, we elucidate the mechanism by which dexamethasone modulates the risks associated with type 2 immune responses. First, we demonstrated that dexamethasone can inhibit both type one and type two cytokine production in Th1 and Th2 cells. In addition, we found that Th2 cells can resist dexamethasone-induced cell apoptosis compared to Th1 and Th0 cells through up-regulating the Bcl-2 anti-apoptotic gene expression to engage the anti-apoptotic response. On the other hand, the ILC2 is still a key lymphocyte for the type 2 immune response, we checked the ILC and ILC2 population in the murine lung and found that ILC2 is a dominant ILC subset in the murine lung. Additionally, the lung-resident ILC and ILC2 present different populations in different genders of the naïve mice. Finally, we found that although dexamethasone could inhibit the type 2 cytokine production of ILC2, it did not induce a significant apoptotic phenomenon on ILC2. In summary, the type 2 immune cells were resistant to dexamethasone-induced cell apoptosis, this phenomenon suggests that the balance between the type 1 and type 2 immunity might impacted by the dexamethasone. | en |
| dc.description.provenance | Submitted by admin ntu (admin@lib.ntu.edu.tw) on 2024-08-16T17:41:07Z No. of bitstreams: 0 | en |
| dc.description.provenance | Made available in DSpace on 2024-08-16T17:41:07Z (GMT). No. of bitstreams: 0 | en |
| dc.description.tableofcontents | Contents
論文口試委員審定書 i Acknowledgment ii 中文摘要 iv Abstract v Contents vi Figure contents x Chapter 1. Introduction 1 Part1. Background 2 1. Asthma 2 1-1. Asthma drugs 3 1-2. β2-agonists 3 1-3. Corticosteroid 4 2. Apoptosis 5 2-1 Extrinsic pathway (death receptor pathway) 6 2-2 Intrinsic pathway (mitochondrial pathway) 6 2-3 Bcl-2(B cell lymphoma 2) protein family in mitochondrial cell apoptosis 7 3. CD4+ T cells 8 3-1 Th1 cells 8 3-2 Th2 cells 9 3-3 Th17 cells 10 4. Innate lymphoid cells 10 4-1. Group one innate lymphoid cells 11 4-2. Group two innate lymphoid cells 12 4-3. Group three innate lymphoid cells 13 5. The effect of asthma drugs on T cells 13 5-1 β2-agonists and the T cells 14 5-2 Corticosteroid and the T cells 14 6. The effect of asthma drugs on ILCs 15 Part2. Statement of the motives 15 Part3. Study aims 17 Chapter2. Materials and Methods 18 Part1. Material 19 1. Animals 19 2. Medium (buffer preparation and cell culture) 19 3. Reagent and buffer 21 4. Antibody 23 5. Cytokine 24 6. Enzyme-linked immunosorbent assay (ELISA) 24 7. Quantitative polymerase chain reaction 26 8. Instrument and software 28 9. Asthma drugs 28 10. Others 28 Part2. Methods 29 1. Murine lung cell isolation 29 2. Murine splenocyte isolation 29 3. Surface marker staining 29 4. CD4+ T cell isolation 30 5. Cell sorting 30 6. T cell differentiation 30 7. ILC2 culture 31 8. Steroid treatment 31 9. β2-agonist treatment 31 10. MTT assay 31 11. Enzyme-linked immunosorbent assay (ELISA) 32 12. Cell apoptosis assay 32 13. RNA extraction 32 14. Reverse transcription polymerase chain reaction 33 15. Real-time PCR 33 16. Statistical analysis 33 Chapter 3. Results 34 1. The CD4+ T cell isolation and differentiation 35 2. Dexamethasone inhibited the CD4+ T cell cytokine production 35 3. The Th2 cells resistant to Dexamethasone-induced cell apoptosis 35 4. The Th2 cells' anti-apoptotic gene expression level upregulated after dexamethasone treatment 36 5. The Th1 but not Th2 cell proliferated gene expression level decreased after dexamethasone treatment 37 6. The IL-4 could not completely rescue the CD4+ T cell survival from dexamethasone-induced cell apoptosis 38 7. The IL-4 could not induce the complete anti-apoptotic gene expression of the CD4+ T cells in the dexamethasone treatment 38 8. The dexamethasone-induced cell proliferated gene down-regulation cannot be reversed by IL-4 treatment 39 9. The IL-12 and IL-4 both rescued the CD4+ T cells in dexamethasone-induced cell apoptosis 39 10. The anti-apoptotic gene of CD4+ T cell up-regulated by IL-4 but not 40 IL-12 in dexamethasone treatment 40 10. The characterization and population of innate lymphoid cells (ILCs) 40 11. The effect of dexamethasone on the ILC2 41 Chapter 4. Discussion 42 Figures 49 References 86 Supplement 100 | - |
| dc.language.iso | en | - |
| dc.subject | 細胞凋亡 | zh_TW |
| dc.subject | Bcl-2家族 | zh_TW |
| dc.subject | 先天性淋巴球 | zh_TW |
| dc.subject | Th2 | zh_TW |
| dc.subject | Th1 | zh_TW |
| dc.subject | Dexamethasone | zh_TW |
| dc.subject | Th1 | en |
| dc.subject | Th2 | en |
| dc.subject | ILC | en |
| dc.subject | Apoptosis | en |
| dc.subject | Bcl-2 family | en |
| dc.subject | Dexamethasone | en |
| dc.title | 類固醇對過敏相關免疫細胞凋亡的影響 | zh_TW |
| dc.title | The Effect of Corticosteroid on Apoptotic Phenomenon of Immune Cells Related to Allergy | en |
| dc.type | Thesis | - |
| dc.date.schoolyear | 112-2 | - |
| dc.description.degree | 碩士 | - |
| dc.contributor.oralexamcommittee | 柯俊榮;莊雅惠 | zh_TW |
| dc.contributor.oralexamcommittee | Chun-Jung Ko;Ya-Hui Chuang | en |
| dc.subject.keyword | Th1,Th2,先天性淋巴球,細胞凋亡,Bcl-2家族,Dexamethasone, | zh_TW |
| dc.subject.keyword | Th1,Th2,ILC,Apoptosis,Bcl-2 family,Dexamethasone, | en |
| dc.relation.page | 102 | - |
| dc.identifier.doi | 10.6342/NTU202403523 | - |
| dc.rights.note | 同意授權(全球公開) | - |
| dc.date.accepted | 2024-08-07 | - |
| dc.contributor.author-college | 醫學院 | - |
| dc.contributor.author-dept | 免疫學研究所 | - |
| 顯示於系所單位： | 免疫學研究所 | |
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