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研究生:林容安
研究生(外文):Jung-An Lin
論文名稱:探討敲除CD4+ T細胞中C1GALT1對類風濕性關節炎小鼠模型的治療效果
論文名稱(外文):To investigate the therapeutic effect of deleting C1GALT1 in CD4+ T cells in a rheumatoid arthritis mouse model
指導教授:林能裕黃敏銓黃敏銓引用關係
指導教授(外文):Neng-Yu LinMin-Chuan Huang
口試委員:郭靜穎莊雅婷
口試委員(外文):Ching-Ying KuoYa-Ting Chuang
口試日期:2023-07-25
學位類別:碩士
校院名稱:國立臺灣大學
系所名稱:解剖學暨細胞生物學研究所
學門:醫藥衛生學門
學類:醫學學類
論文種類:學術論文
論文出版年:2023
畢業學年度:111
論文頁數:94
中文關鍵詞:Core 1 synthaseCD4+ T cell膠原抗體誘導性關節炎模型T 細胞分化
外文關鍵詞:Core 1 synthaseCD4+ T cellCollagen Antibody-Induced Arthritis
DOI:10.6342/NTU202303703
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類風濕性關節炎(Rheumatoid arthritis, RA)是一種慢性自體免疫疾病,由關節滑膜的慢性發炎所引起。RA的發病機制涉及T細胞的活化和促發炎因子的分泌,如GM-CSF、IL-17A、IL-17F和IL-23等,這些促發炎因子促進Th17細胞分化和增值,導致軟骨侵蝕、硬骨侵蝕以及免疫細胞浸潤,最終導致關節結構受損。近年研究發現異常的醣基化與自體免疫疾病的誘發有關,C1GALT1 (Core 1 beta1,3-galactosyltransferase, Core 1 synthase) 是使氧型醣基化中的醣類結構產生分支和複雜度的關鍵酵素。然而,C1GALT1在RA發病機制中的調控機制和影響仍不清楚。本研究旨在探討C1GALT1在RA發病機制中的作用以及對T細胞分化的影響。首先,我們使用免疫組織化學染色法分析了膠原抗體誘導性關節炎(Collagen Antibody-Induced Arthritis, CAIA)小鼠脾臟中C1GALT1的蛋白表達,結果顯示C1GALT1在發炎反應中表達增加。而為了進一步探討C1GALT1對T細胞分化的影響,我們繁殖出了C1GALT1f/f CD4-Cre (C1GALT1 KO)小鼠,其C1GALT1基因在naïve T細胞分化為CD4+ T細胞的過程中被敲除,從而影響CD4+ T 細胞表面醣類結構的修飾。流式細胞儀分析C1GALT1f/f和C1GALT1 KO小鼠的脾臟、胸腺和淋巴結,發現敲除C1GALT1基因後VVA lectin(Vicia Villosa Lectin)的表達增加,表明CD4+ T細胞表面醣類結構發生了改變。此外,在小鼠誘導關節炎的實驗中發現,CD4+ T細胞特異性敲除C1GALT1改善了小鼠的踝關節腫脹、爪力強度以及臨床評分。並在骨表面掃描結果顯示C1GALT1 KO小鼠的腳掌骨表面骨侵蝕減緩。這些研究結果表明,在CAIA關節炎模型中,CD4+ T細胞特異性敲除C1GALT1可能減輕關節發炎所引起的踝關節腫脹,說明C1GALT1或許具有抑制發炎的潛力。瞭解C1GALT1在RA發病機制和T細胞分化中的作用,可以有助於提供醣基化治療RA和其他自體免疫疾病的方法。
Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by chronic inflammation targeting synovial membrane in the joints, resulting in arthritis. The pathogenesis of RA involves T cell activation and the secretion of proinflammatory cytokines, such as GM-CSF, IL-17A, IL-17F, and IL-23. These proinflammatory cytokines promote T cell differentiation and proliferation, leading to cartilage and bone erosion, and immune cell infiltration, which ultimately result in damage to joint structures. Abnormal glycosylation has also been implicated in autoimmune diseases, with the glycosyltransferase C1GALT1 playing a critical role in O-glycosylation and glycan complexity. However, the regulatory mechanisms and impact of C1GALT1 on RA pathogenesis remain unclear. This study aimed to investigate the role of C1GALT1 in RA pathogenesis and its effect on T differentiation. Initially, we analyzed the protein expression of C1GALT1 in the spleens of Collagen Antibody-Induced Arthritis (CAIA) induced C57BL/6 mice using immunohistochemistry, revealing increased C1GALT1 expression in response to inflammation. To explore the influence of C1GALT1 on Th17 differentiation, we generated C1GALT1f/f CD4-Cre mice (C1GALT1 KO), in which the C1GALT1 gene was knocked out during the differentiation of naïve T cells into CD4+ T cells, impacting surface glycan modification. Flow cytometry analysis of spleens, thymus, and lymph nodes from C1GALT1f/f and C1GALT1f/f CD4-Cre mice showed increased lectin expression of VVA following C1GALT1 gene knockout, indicating altered O-glycans on the surface of CD4+ T cells. Furthermore, we employed the CAIA model to simulate RA in mice and compared C1GALT1f/f CD4-Cre mice to C1GALT1f/f mice. The results demonstrated that C1GALT1 knockout in T cells alleviated ankle swelling in the CAIA model, with reduced swelling observed from Day 6 to Day 10. Additionally, bone scan analysis revealed a deceleration of bone erosion on the paw bone surface in C1GALT1 KO. These findings suggest that T cell-specific knockout of C1GALT1 may mitigate ankle swelling in the CAIA model, emphasizing the crucial role of C1GALT1 in suppressing inflammation. Understanding the role of C1GALT1 in RA pathogenesis and T cell differentiation could provide insights into potential therapeutic strategies targeting glycosylation pathways for the treatment of RA and other autoimmune diseases.
口試委員會審定書 ⅰ
致謝 ⅰi
中文摘要 ⅰii
Abstract iv
Abbreviation v
Chapter 1 Introductions 1
1.1 Autoimmune disease 1
1.1.1 The definition of autoimmune diseases 1
1.1.2 Rheumatoid arthritis 1
1.1.3 The prevalence and diagnostic methods of rheumatoid arthritis 2
1.1.4 The mechanisms of rheumatoid arthritis 2
1.1.5 Treatment strategies and challenges in rheumatoid arthritis 4
1.2 Glycosylation 7
1.2.1 The definition and biological functions of glycosylation 7
1.2.2 The type of glycosylation 7
1.2.3 Glycosylation and immunity 9
1.3 Mouse models that mimic the pathogenesis of human RA 11
1.3.1 Collagen Antibody-Induced Arthritis (CAIA) model 11
1.3.2 K/BxN serum-transfer arthritis (STA) model 12
1.4 Research value of C1GALT1 in autoimmune diseases 13
Chapter 2 Study objectives and Hypotheses 15
Chapter 3 Materials and Methods 18
3.1 Materials 18
3.1.1 Antibody 18
3.1.2 Primers 19
3.1.3 Chemical and Reagents 19
3.1.3.1 Buffer Solutions and Reagents 22
3.1.4 Instruments and Software 26
3.2 Methods 28
3.2.1 Mice primary cells isolation 28
3.2.2 Animal Handling 28
3.2.3 Tissue Decalcification 29
3.2.4 Immunohistochemistry staining 29
3.2.5 Tartrate resistant acid phosphatase staining (TRAP) 30
3.2.6 Toluidine Blue Staining 30
3.2.7 Flow cytometry 31
3.2.8 Bradford protein assay 31
3.2.9 Western blot 32
3.2.10 Collagen Antibody-Induced Arthritis model (CAIA) 32
3.2.11 CAIA clinical arthritis score 33
3.2.12 K/BxN Serum-Transfer Arthritis model (K/BxN STA) 33
3.2.13 K/BxN STA clinical arthritis score 33
3.2.14 Malleoli size measurements 34
3.2.15 Grip strength measurements 34
3.2.16 Toluidine blue staining histopathological scoring 35
3.2.17 H&E staining histopathological scoring 35
3.2.18 TRAP-positive osteoclasts counting 36
3.2.19 Trajectory analysis 36
3.2.20 Bone surface erosion by micro CT analysis 36
3.2.21 Mouse TNF-α Enzyme-linked immunosorbent assay 37
3.2.22 Statistical analysis 37
Chapter 4 Result 38
4.1 C1GALT1 increase during collagen antibody-induced arthritis mouse model 38
4.2 Generation of C1GALT1 conditional knockdout mice for study the mechanisms of RA 38
4.2.1 The impact of knockout C1GALT1 in mouse thymus on immune organs 38
4.2.2 The impact of knockout C1GALT1 in mouse thymus on cell surface glycan structures 39
4.2.3 The impact of knockout C1GALT1 on the population of CD4+ T cells, CD8+ T cells, and B cells in mouse immune organs 39
4.3 C1GALT1f/f CD4+Cre mice alleviate the clinical index in CAIA 41
4.3.1 C1GALT1f/f CD4+Cre mice showed improvement in weight loss during CAIA 41
4.3.2 C1GALT1f/f CD4+Cre mice showed alleviated ankle swelling during CAIA 41
4.3.3 C1GALT1f/f CD4+Cre mice alleviated the functional decline in joint inflammation induced by CAIA 42
4.3.4 C1GALT1f/f CD4+Cre mice exhibited reduced paw swelling scores during CAIA 42
4.3.5 C1GALT1f/f CD4+Cre mice did not exhibit any improvement in walking distance and velocity of the mice in CAIA 43
4.4 C1GALT1f/f CD4+Cre mice alleviate the histopathological scoring in CAIA 43
4.4.1 C1GALT1f/f CD4+Cre mice exhibited amelioration of cartilage erosion and proteoglycan loss in the CAIA model 43
4.4.2 C1GALT1f/f CD4+Cre mice exhibited amelioration of bone erosion in the CAIA model 44
4.4.3 C1GALT1f/f CD4+Cre mice showed reduced inflammation activity and synovial lining hyperplasia in the CAIA model 45
4.5 The level of TNF-α in the serum of C1GALT1f/f CD4+Cre mice is decreased 45
4.6 The population of CD3+ T cells, CD4+ T cells and CD8+ T cells are decreased in the spleen and lymph nodes of C1GALT1f/f CD4+Cre mice 46
4.7 C1GALT1 increase during K/BxN Serum-Transfer Arthritis model 47
4.8 C1GALT1f/f CD4+Cre mice alleviate the clinical index in K/BxN STA 47
4.8.1 C1GALT1f/f CD4+Cre mice improvement in weight loss during K/BxN STA 47
4.8.2 C1GALT1f/f CD4+Cre mice alleviated ankle swelling during K/BxN STA 48
4.8.3 C1GALT1f/f CD4+Cre mice alleviated the functional decline in joint inflammation induced by K/BxN STA 48
4.8.4 C1GALT1f/f CD4+Cre mice exhibited reduced paw swelling scores during K/BxN STA 49
4.9 C1GALT1f/f CD4+Cre mice alleviate the histopathological scoring in K/BxN STA 49
4.9.1 C1GALT1f/f CD4+Cre mice exhibited amelioration of cartilage erosion and proteoglycan loss in the K/BxN STA model 49
4.9.2 C1GALT1f/f CD4+Cre mice exhibited amelioration of bone erosion in the K/BxN STA model 50
4.9.3 C1GALT1f/f CD4+Cre mice reduced inflammation activity and synovial lining hyperplasia in the K/BxN STA model 51
Chapter 5 Conclusion 53
Chapter 6 Discussion 54
6.1 Knockout of C1GALT1 did not improve walking distance and velocity in arthritic mice 54
6.2 Knockout of C1GALT1 in CD4+ T cell resulted in a decreased population of CD3+ T cells, CD4+ T cells and CD8+ T cells in the spleen and lymph nodes 54
References 56
List of Tables 65
List of Figures 67
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