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帶血管骨髓及調節性T細胞在誘導及維持異體複合移植物免疫耐受上所扮演的重要角色

為了解決Mazda maintenance bo的問題，作者雷安琪 這樣論述：

TABLE OF CONTENTS口試委員會審定書指導教授推薦書ACKNOWLEDGEMENTS iiiCHINESE ABSTRACT vENGLISH ABSTRACT viTABLE OF CONTENTS viiiLIST OF TABLES xiiLIST OF FIGURES xiiiABBREVIATIONS xviiiI. INTRODUCTION 1I. I. Transplantation 1I. II. Vascularized Composite Allograft 1I. III.

Immune System and Allograft Rejection 2I. IV. Concept for Transplant Tolerance 4I.IV. I. Chimerism 4I.IV. II. Immunosuppression Drug 5I.IV. III. Blocking Antibody 5I.IV. IV. Cell Therapy 6I. V. Time Line of Strategy to induce VCA Tolerance 7II. Aims and Hypo

thesis 10III. METHODS 11III. I. Mice 11III. II. Experimental Design 11III. III. Vascularized Composite Allotransplantation Model (Heterotopic Hindlimb Transplantation) with Neck as Preferred Site 13III. IV. Care During and Post Surgery 14III. V. Immunosuppression

Drug Regimens 14III. VI. Bone Marrow Transplantations 14III. VII. CD25 Depleting Treatment 15III. VIII. Clinical Assessment and Allograft Monitoring 15III. IX. Bone Removal 15III. X. Skin Grafting 15III. XI. Real-Time PCR 15III. XII. Analysis of Peripheral B

lood Cell 16III. XIII. Analysis of IL-10 Level in the Serum 16III. XIV. Immunohistochemical Staining 17III.XIV I. Hematoxylin 17III.XIV II. Immunohistochemistry 17III. XV. Magnetic Cell Separation for MLR or Adoptive Transfer 18III. XVI. Mixed Lymphocytes Reaction

18III. XVII. Tregs Suppressive Assay 19III. XVIII. Tregs Adoptive Transfer 19III. XIX. Statistical Analysis 20IV. RESULTS 21IV. I. Efficacy of CBMT and VBM Transplantation to Prolong Allograft Survival in Transplanted Mice under CoB and Short-term Rapamycin 21IV. II

. Chimerism Level in CBMT and VBM Transplantation Recipient 21IV. III. Composition of Donor Cells in Multiple Lymphoid Organ and Bone of CBMT and VBM Transplantation Recipient 22IV. IV. Donor Reactive T cells were Suppressed in VBM Transplantation Recipients. 23IV. V.

CD4+ and CD8+ cells from Recipients with Long-term Surviving Grafts demonstrated Donor-specific Hyporesponsiveness In Vitro in an MLR assay 23IV. VI. Duration the Presence of VBM to Maintain Donor-specific Tolerance to Secondary Skin Graft Transplantation 24IV. VII. Balance Ratio of Tr

eg/ Teff in Transplanted Mice under CoB and Short-term Rapamycin 24IV. VIII. Tregs of tolerant recipients showed higher expression of activation markers and cytokines early post-op 25IV. IX. The Critical Timing of Tregs Presence 25IV. X. Tolerance was Established at Late Stage of T

ransplantation 26IV. XI. Tregs Engraftment in Allograft 26IV. XII. Tregs Capability to Donor-specific Targeted Cell 27IV. XIII. Low Percentage of Donor-derived CD4+CD25+FOXP3+ Tregs was Found in VCA Recipients 27IV. XIV. The Ability of Tregs to Improve Allograft Outcome 28

V. Discussion 29V. I. Role of Vascularized Bone Marrow 29V. II. Role of Regulatory T Cells 32VI. CONCLUSION AND FUTURE PROSPECT 38REFERENCES 39TABLE 51FIGURE 53Appendix 97 LIST OF TABLESTable 1. Grouping for CBMT versus VBM Transplantation 51Table 2. Grouping f

or Tregs study 51Table 3. Primer List 52 LIST OF FIGURESFigure 1. Monitoring immune response at pre- and post- Tregs depletion. Tregs were depleted for 60 days. 53Figure 2. Immunosuppression protocol. 54Figure 3. Characterization of cell population after Tregs purification using mouse CD

4+CD25+ isolation kit. 54Figure 4. Percentage of Tregs in the peripheral blood at pre- and 3 days post- Tregs adoptively transferred 55Figure 5. VBM transplantation with CoB and RPM resulted in prolonged VCA survival 56Figure 6. Leukocyte chimerism in the peripheral blood of recipients amon

g different groups at POD 30 of high CBMT, low CBMT and VBM transplantation recipients with long-term VCA survival 120 days following transplantation 57Figure 7. Grouped data of multilineage chimerism of high CBMT, low CBMT and VBM transplantation recipients with long-term VCA survival 120 days f

ollowing transplantation 58Figure 8. Subpopulation of lymphoid cells in peripheral blood of high CBMT, low CBMT and VBM transplantation recipients with long-term VCA survival 120 days following transplantation 59Figure 9. Immunohistochemical staining of MHC class II donor cells (IAd) in the th

ymus, lymph node, and spleen of VCA recipients collected at POD 120 or at the time of rejection 60Figure 10. Flowcytometry analysis of donor cells (H2d) resided in the thymus, bone, lymph node and spleen of VCA recipients 61Figure 11. Changes in specific peripheral cell populations were mainta

ined in VBM transplantation recipients 62Figure 12. CD4+ and CD8+ cells from recipients with long-term surviving grafts demonstrated donor-specific hyporesponsiveness in vitro in an MLR assay 63Figure 13. Timeline of OMC flap removal following skin transplantation 64Figure 14. Secondary ski

n graft was viable at 60 days post OMC flap removal 65Figure 15. Robust tolerance of the skin allograft (> 60 days) was not affected by timing of OMC flap removal (POD 30, 60 or 120) 66Figure 16. Removal of OMC flap at different time points did not affect the graft survival 67Figure 17. Per

ipheral chimerism was not detected after flap removal 68Figure 18. Percentage of peripheral lymphocytes after removal of OMC flap did not change significantly 69Figure 19. Ratio of Tregs to CD4+ and CD8+ T cell in total lymphocytes 70Figure 20. Ratio of Tregs to Teff subtypes in total CD4 T

cells 71Figure 21. Longitudinal assessment of expression of GITR, GATA3 and Tbet of Tregs from tolerant and rejected mice 72Figure 22. Longitudinal assessment of the levels of expression of TGF-β, IL-10 and IL-35 of Tregs from tolerant and rejected mice 73Figure 23. Longitudinal assessment

of the levels of IL-10 in serum 74Figure 24. Depletion Treg in early stage of transplantation affects robust tolerant 75Figure 25. Tregs adoptively transferred after Treg depletion was prevent the allograft rejection 76Figure 26. Expression of TCR Vβ5 on CD4+ T cells in the peripheral bloo

d after Treg depletion 76Figure 27. CD4+ and CD8+ T cells hyporesponsiveness in the recipient with Treg depletion 77Figure 28. Donor specific antibodies secretion in the recipient with Treg depletion 77Figure 29. Representative contour plot of flowcytometry analysis from accumulation of Fox

P3+ cells n drain lymph node and long-term accepted graft (tolerant) 78Figure 30. Allograft harvested at the experimental endpoints (POD 180 or at the time point of rejection) 79Figure 31. Absolute number of Tregs cells in lymphoid organs and skin of OMC of tolerant at the time of rejection an

d rejection recipients at POD 180 by flowcytometry 80Figure 32. Hematoxylin-eosin and FoxP3+ IHC staining. 81Figure 33. Relative mRNA FoxP3 expression 82Figure 34. Skin paddled allografts from tolerant recipients at POD 180 were transplanted onto Rag2-/- and monitored for 60 days 83F

igure 35. Monitoring T cell population in the peripheral blood at POD 30 after skin-paddled allografts from tolerant recipients at POD 180 were transplanted onto Rag2-/- 84Figure 36. Graft survival in Rag2-/- transplanted recipients with and without Teff adoptively transferred 85Figure 37.

CD3+ T cells proliferation after 4 days co-culture with Tregs from tolerant recipients at various ratios 86Figure 38. Representative dot plot and histogram from Tregs assay where CD3+ T cells proliferation after 4 days co-culture with Tregs from tolerant and rejected recipients at ratio 1:1 8

7Figure 39. CD3+ T cells proliferation after 4 days co-culture with Tregs from tolerant and rejected recipients at ratio 1:1 88Figure 40. GFP+CD4+CD25+FOXP3+ regulatory cells detection from peripheral blood 89Figure 41. GFP+CD4+CD25+FOXP3+ regulatory cells detection from secondary lymphoid

90Figure 42. Immunohistochemistry of GFP+CD4+CD25+FOXP3+ regulatory cells detected in skin of OMC 91Figure 43. Number of GFP+CD4+CD25+FOXP3+ regulatory cells detected in skin of OMC 92Figure 44. CD8+FOXP3+ regulatory cells detection from peripheral blood 93Figure 45. B regulatory ce

lls detection from peripheral blood 94Figure 46. Adoptively transferred 2x106 of Tregs that were isolated from tolerant and Naïve into VCA recipient mice that were injected with anti-CD25 at POD 30 mice via tail vein at POD 60 (n=3) prevent rejection 95Figure 47. Mechanism of induction and mai

ntenance tolerance in VCA 96

艾葉所含具選擇性抑制Podoplanin所誘導之血小板凝集的多醣體研究

為了解決Mazda maintenance bo的問題，作者黃鈺淩 這樣論述：

腫瘤的轉移 (metastasis) 是造成癌症高死亡率及治療困難的主要原因。腫瘤在血源性轉移 (haematogenous metastasis) 的過程中，會誘導血小板活化與凝集，進而與血小板產生交互作用，稱之為 「腫瘤細胞誘導血小板凝集反應」 (tumor cell-induced platelet aggregation, TCIPA)，此反應被證實與腫瘤細胞轉移有高度正相關，因此抑制血小板凝集與 TCIPA 反應具抑制腫瘤細胞轉移之潛力。有文獻指出，血小板抗凝劑如 aspirin 可抑制 TCIPA，但因缺乏選擇性而會影響人體正常凝血功能。近年來發現一個廣泛存在於在惡性腫瘤細胞表面

之醣蛋白 podoplanin (PDPN)，可透過與血小板表面的 C 型類凝集素接受體 c-type lectin-like receptor 2 (CLEC-2) 專一性結合，進而活化血小板並提高發生 TCIPA 之機率，而將此途徑阻斷則可減少腫瘤細胞轉移及惡性腫瘤發生之機率，且不會影響人體正常凝血功能，因此 CLEC-2 與 PDPN 之專一性結合將有機會成為治療癌症轉移極具潛力的分子標靶。本研究首先評估一系列中草藥水萃物對於 rPDPN、collagen、thrombin、U46619 所誘導之血小板凝集反應之抑制活性後，篩選出艾葉水萃物作為候選藥物 (candidate herb)。

接著依據生物活性導引法 (bioactivity-guided fractionation) 分離並純化出可專一且有效抑制 PDPN 誘導血小板凝集之成分或劃分層，最後再進行此有效成分或劃分層之定性與定量分析。研究結果顯示，艾葉含多醣之高分子量酸不可溶性活性劃分層 (CHE-3-WPUU-AP) 會藉由不可逆性的非競爭型抑制 PDPN 與 CLEC-2 之結合，進而抑制血小板 CLEC-2 下游蛋白質之磷酸化，因而可專一性抑制 PDPN 誘導之血小板凝集反應及 TCIPA，且對血小板及腫瘤細胞均無明顯毒性，因此認為艾葉之酸不可溶性多醣體具備減少腫瘤轉移藥物之開發潛力。