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完整後設資料紀錄
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.advisor | 莊雅惠 | |
dc.contributor.author | Teng-Yuan Wei | en |
dc.contributor.author | 韋登元 | zh_TW |
dc.date.accessioned | 2021-06-17T01:18:56Z | - |
dc.date.available | 2027-12-31 | |
dc.date.copyright | 2017-09-14 | |
dc.date.issued | 2017 | |
dc.date.submitted | 2017-08-11 | |
dc.identifier.citation | 1. Ermann, J. and C.G. Fathman, Autoimmune diseases: genes, bugs and failed regulation. Nat Immunol, 2001. 2(9): p. 759-61.
2. Wahren-Herlenius, M. and T. Dorner, Immunopathogenic mechanisms of systemic autoimmune disease. Lancet, 2013. 382(9894): p. 819-31. 3. Yang, J., et al., Th17 and natural Treg cell population dynamics in systemic lupus erythematosus. Arthritis Rheum, 2009. 60(5): p. 1472-83. 4. Shivakumar, S., G.C. Tsokos, and S.K. Datta, T cell receptor alpha/beta expressing double-negative (CD4-/CD8-) and CD4+ T helper cells in humans augment the production of pathogenic anti-DNA autoantibodies associated with lupus nephritis. J Immunol, 1989. 143(1): p. 103-12. 5. Crispin, J.C., et al., Expanded double negative T cells in patients with systemic lupus erythematosus produce IL-17 and infiltrate the kidneys. J Immunol, 2008. 181(12): p. 8761-6. 6. Futatsugi-Yumikura, S., et al., Pathogenic Th2-type follicular helper T cells contribute to the development of lupus in Fas-deficient mice. Int Immunol, 2014. 26(4): p. 221-31. 7. Bonelli, M., et al., Quantitative and qualitative deficiencies of regulatory T cells in patients with systemic lupus erythematosus (SLE). Int Immunol, 2008. 20(7): p. 861-8. 8. Vargas-Rojas, M.I., et al., Quantitative and qualitative normal regulatory T cells are not capable of inducing suppression in SLE patients due to T-cell resistance. Lupus, 2008. 17(4): p. 289-94. 9. Smolen, J.S., D. Aletaha, and I.B. McInnes, Rheumatoid arthritis. Lancet, 2016. 388(10055): p. 2023-2038. 10. Nakae, S., et al., Suppression of immune induction of collagen-induced arthritis in IL-17-deficient mice. J Immunol, 2003. 171(11): p. 6173-7. 11. Hata, H., et al., Distinct contribution of IL-6, TNF-alpha, IL-1, and IL-10 to T cell-mediated spontaneous autoimmune arthritis in mice. J Clin Invest, 2004. 114(4): p. 582-8. 12. Kotake, S., et al., IL-17 in synovial fluids from patients with rheumatoid arthritis is a potent stimulator of osteoclastogenesis. J Clin Invest, 1999. 103(9): p. 1345-52. 13. Katz, Y., O. Nadiv, and Y. Beer, Interleukin-17 enhances tumor necrosis factor alpha-induced synthesis of interleukins 1,6, and 8 in skin and synovial fibroblasts: a possible role as a 'fine-tuning cytokine' in inflammation processes. Arthritis Rheum, 2001. 44(9): p. 2176-84. 14. McMahon, E.J., et al., Epitope spreading initiates in the CNS in two mouse models of multiple sclerosis. Nat Med, 2005. 11(3): p. 335-9. 15. Lovett-Racke, A.E., Y. Yang, and M.K. Racke, Th1 versus Th17: are T cell cytokines relevant in multiple sclerosis? Biochim Biophys Acta, 2011. 1812(2): p. 246-51. 16. Kozovska, M.E., et al., Interferon beta induces T-helper 2 immune deviation in MS. Neurology, 1999. 53(8): p. 1692-7. 17. Zoghi, S., et al., Cytokine secretion pattern in treatment of lymphocytes of multiple sclerosis patients with fumaric acid esters. Immunol Invest, 2011. 40(6): p. 581-96. 18. Neumann, H., et al., Cytotoxic T lymphocytes in autoimmune and degenerative CNS diseases. Trends Neurosci, 2002. 25(6): p. 313-9. 19. Ji, Q., L. Castelli, and J.M. Goverman, MHC class I-restricted myelin epitopes are cross-presented by Tip-DCs that promote determinant spreading to CD8(+) T cells. Nat Immunol, 2013. 14(3): p. 254-61. 20. Jen, H.Y., et al., Increased serum interleukin-17 and peripheral Th17 cells in children with acute Henoch-Schonlein purpura. Pediatr Allergy Immunol, 2011. 22(8): p. 862-8. 21. Chen, O., et al., The imbalance of Th17/Treg in Chinese children with Henoch-Schonlein purpura. Int Immunopharmacol, 2013. 16(1): p. 67-71. 22. Rosenblum, M.D., et al., Treating human autoimmunity: current practice and future prospects. Sci Transl Med, 2012. 4(125): p. 125sr1. 23. Pittenger, M.F., et al., Multilineage potential of adult human mesenchymal stem cells. Science, 1999. 284(5411): p. 143-7. 24. Muguruma, Y., et al., Reconstitution of the functional human hematopoietic microenvironment derived from human mesenchymal stem cells in the murine bone marrow compartment. Blood, 2006. 107(5): p. 1878-87. 25. Horwitz, E.M., et al., Clarification of the nomenclature for MSC: The International Society for Cellular Therapy position statement. Cytotherapy, 2005. 7(5): p. 393-5. 26. Nauta, A.J., et al., Mesenchymal stem cells inhibit generation and function of both CD34+-derived and monocyte-derived dendritic cells. J Immunol, 2006. 177(4): p. 2080-7. 27. Spaggiari, G.M., et al., Mesenchymal stem cells inhibit natural killer-cell proliferation, cytotoxicity, and cytokine production: role of indoleamine 2,3-dioxygenase and prostaglandin E2. Blood, 2008. 111(3): p. 1327-33. 28. Raffaghello, L., et al., Human mesenchymal stem cells inhibit neutrophil apoptosis: a model for neutrophil preservation in the bone marrow niche. Stem Cells, 2008. 26(1): p. 151-62. 29. Traggiai, E., et al., Bone marrow-derived mesenchymal stem cells induce both polyclonal expansion and differentiation of B cells isolated from healthy donors and systemic lupus erythematosus patients. Stem Cells, 2008. 26(2): p. 562-9. 30. Corcione, A., et al., Human mesenchymal stem cells modulate B-cell functions. Blood, 2006. 107(1): p. 367-72. 31. Yoo, H.S., et al., Mesenchymal stromal cells inhibit CD25 expression via the mTOR pathway to potentiate T-cell suppression. Cell Death Dis, 2017. 8(2): p. e2632. 32. Glennie, S., et al., Bone marrow mesenchymal stem cells induce division arrest anergy of activated T cells. Blood, 2005. 105(7): p. 2821-7. 33. Aggarwal, S. and M.F. Pittenger, Human mesenchymal stem cells modulate allogeneic immune cell responses. Blood, 2005. 105(4): p. 1815-22. 34. Lim, J.H., et al., Immunomodulation of delayed-type hypersensitivity responses by mesenchymal stem cells is associated with bystander T cell apoptosis in the draining lymph node. J Immunol, 2010. 185(7): p. 4022-9. 35. Gonzalez, M.A., et al., Adipose-derived mesenchymal stem cells alleviate experimental colitis by inhibiting inflammatory and autoimmune responses. Gastroenterology, 2009. 136(3): p. 978-89. 36. Boumaza, I., et al., Autologous bone marrow-derived rat mesenchymal stem cells promote PDX-1 and insulin expression in the islets, alter T cell cytokine pattern and preserve regulatory T cells in the periphery and induce sustained normoglycemia. J Autoimmun, 2009. 32(1): p. 33-42. 37. Kavanagh, H. and B.P. Mahon, Allogeneic mesenchymal stem cells prevent allergic airway inflammation by inducing murine regulatory T cells. Allergy, 2011. 66(4): p. 523-31. 38. Zhou, H., et al., Efficacy of bone marrow-derived mesenchymal stem cells in the treatment of sclerodermatous chronic graft-versus-host disease: clinical report. Biol Blood Marrow Transplant, 2010. 16(3): p. 403-12. 39. Fiorina, P., et al., Immunomodulatory function of bone marrow-derived mesenchymal stem cells in experimental autoimmune type 1 diabetes. J Immunol, 2009. 183(2): p. 993-1004. 40. Ghannam, S., et al., Mesenchymal stem cells inhibit human Th17 cell differentiation and function and induce a T regulatory cell phenotype. J Immunol, 2010. 185(1): p. 302-12. 41. Rafei, M., et al., Mesenchymal stromal cells ameliorate experimental autoimmune encephalomyelitis by inhibiting CD4 Th17 T cells in a CC chemokine ligand 2-dependent manner. J Immunol, 2009. 182(10): p. 5994-6002. 42. Darlington, P.J., et al., Reciprocal Th1 and Th17 regulation by mesenchymal stem cells: Implication for multiple sclerosis. Ann Neurol, 2010. 68(4): p. 540-5. 43. Li, M., et al., Mesenchymal stem cells suppress CD8+ T cell-mediated activation by suppressing natural killer group 2, member D protein receptor expression and secretion of prostaglandin E2, indoleamine 2, 3-dioxygenase and transforming growth factor-beta. Clin Exp Immunol, 2014. 178(3): p. 516-24. 44. Rasmusson, I., et al., Mesenchymal stem cells fail to trigger effector functions of cytotoxic T lymphocytes. J Leukoc Biol, 2007. 82(4): p. 887-93. 45. Rasmusson, I., et al., Mesenchymal stem cells inhibit the formation of cytotoxic T lymphocytes, but not activated cytotoxic T lymphocytes or natural killer cells. Transplantation, 2003. 76(8): p. 1208-13. 46. Karlsson, H., et al., Mesenchymal stem cells exert differential effects on alloantigen and virus-specific T-cell responses. Blood, 2008. 112(3): p. 532-41. 47. Selmani, Z., et al., Human leukocyte antigen-G5 secretion by human mesenchymal stem cells is required to suppress T lymphocyte and natural killer function and to induce CD4+CD25highFOXP3+ regulatory T cells. Stem Cells, 2008. 26(1): p. 212-22. 48. Augello, A., et al., Bone marrow mesenchymal progenitor cells inhibit lymphocyte proliferation by activation of the programmed death 1 pathway. Eur J Immunol, 2005. 35(5): p. 1482-90. 49. Krampera, M., et al., Role for interferon-gamma in the immunomodulatory activity of human bone marrow mesenchymal stem cells. Stem Cells, 2006. 24(2): p. 386-98. 50. Ryan, J.M., et al., Interferon-gamma does not break, but promotes the immunosuppressive capacity of adult human mesenchymal stem cells. Clin Exp Immunol, 2007. 149(2): p. 353-63. 51. Di Nicola, M., et al., Human bone marrow stromal cells suppress T-lymphocyte proliferation induced by cellular or nonspecific mitogenic stimuli. Blood, 2002. 99(10): p. 3838-43. 52. Renner, P., et al., Mesenchymal stem cells require a sufficient, ongoing immune response to exert their immunosuppressive function. Transplant Proc, 2009. 41(6): p. 2607-11. 53. Li, W., et al., Mesenchymal stem cells: a double-edged sword in regulating immune responses. Cell Death Differ, 2012. 19(9): p. 1505-13. 54. Romieu-Mourez, R., et al., Cytokine modulation of TLR expression and activation in mesenchymal stromal cells leads to a proinflammatory phenotype. J Immunol, 2009. 182(12): p. 7963-73. 55. Waterman, R.S., et al., A new mesenchymal stem cell (MSC) paradigm: polarization into a pro-inflammatory MSC1 or an Immunosuppressive MSC2 phenotype. PLoS One, 2010. 5(4): p. e10088. 56. Stagg, J., et al., Interferon-gamma-stimulated marrow stromal cells: a new type of nonhematopoietic antigen-presenting cell. Blood, 2006. 107(6): p. 2570-7. 57. Chan, J.L., et al., Antigen-presenting property of mesenchymal stem cells occurs during a narrow window at low levels of interferon-gamma. Blood, 2006. 107(12): p. 4817-24. 58. Tse, W.T., et al., Suppression of allogeneic T-cell proliferation by human marrow stromal cells: implications in transplantation. Transplantation, 2003. 75(3): p. 389-97. 59. Rustad, K.C. and G.C. Gurtner, Mesenchymal Stem Cells Home to Sites of Injury and Inflammation. Adv Wound Care (New Rochelle), 2012. 1(4): p. 147-152. 60. Amorin, B., et al., Mesenchymal stem cell therapy and acute graft-versus-host disease: a review. Hum Cell, 2014. 27(4): p. 137-50. 61. Liang, J., et al., Allogenic mesenchymal stem cells transplantation in refractory systemic lupus erythematosus: a pilot clinical study. Ann Rheum Dis, 2010. 69(8): p. 1423-9. 62. Llufriu, S., et al., Randomized placebo-controlled phase II trial of autologous mesenchymal stem cells in multiple sclerosis. PLoS One, 2014. 9(12): p. e113936. 63. Forbes, G.M., et al., A phase 2 study of allogeneic mesenchymal stromal cells for luminal Crohn's disease refractory to biologic therapy. Clin Gastroenterol Hepatol, 2014. 12(1): p. 64-71. 64. Su, L.J., et al., Fluorescent nanodiamonds enable quantitative tracking of human mesenchymal stem cells in miniature pigs. Sci Rep, 2017. 7: p. 45607. 65. Schmitz, J., et al., IL-33, an interleukin-1-like cytokine that signals via the IL-1 receptor-related protein ST2 and induces T helper type 2-associated cytokines. Immunity, 2005. 23(5): p. 479-90. 66. Moussion, C., N. Ortega, and J.P. Girard, The IL-1-like cytokine IL-33 is constitutively expressed in the nucleus of endothelial cells and epithelial cells in vivo: a novel 'alarmin'? PLoS One, 2008. 3(10): p. e3331. 67. Lefrancais, E., et al., IL-33 is processed into mature bioactive forms by neutrophil elastase and cathepsin G. Proc Natl Acad Sci U S A, 2012. 109(5): p. 1673-8. 68. Lefrancais, E., et al., Central domain of IL-33 is cleaved by mast cell proteases for potent activation of group-2 innate lymphoid cells. Proc Natl Acad Sci U S A, 2014. 111(43): p. 15502-7. 69. Luthi, A.U., et al., Suppression of interleukin-33 bioactivity through proteolysis by apoptotic caspases. Immunity, 2009. 31(1): p. 84-98. 70. Molofsky, A.B., A.K. Savage, and R.M. Locksley, Interleukin-33 in Tissue Homeostasis, Injury, and Inflammation. Immunity, 2015. 42(6): p. 1005-19. 71. Morita, H., et al., An Interleukin-33-Mast Cell-Interleukin-2 Axis Suppresses Papain-Induced Allergic Inflammation by Promoting Regulatory T Cell Numbers. Immunity, 2015. 43(1): p. 175-86. 72. Zaiss, D.M., et al., Emerging functions of amphiregulin in orchestrating immunity, inflammation, and tissue repair. Immunity, 2015. 42(2): p. 216-26. 73. Baumann, C., et al., T-bet- and STAT4-dependent IL-33 receptor expression directly promotes antiviral Th1 cell responses. Proc Natl Acad Sci U S A, 2015. 112(13): p. 4056-61. 74. Liew, F.Y., J.P. Girard, and H.R. Turnquist, Interleukin-33 in health and disease. Nat Rev Immunol, 2016. 16(11): p. 676-689. 75. Ren, G., et al., Mesenchymal stem cell-mediated immunosuppression occurs via concerted action of chemokines and nitric oxide. Cell Stem Cell, 2008. 2(2): p. 141-50. 76. Meisel, R., et al., Human bone marrow stromal cells inhibit allogeneic T-cell responses by indoleamine 2,3-dioxygenase-mediated tryptophan degradation. Blood, 2004. 103(12): p. 4619-21. 77. Le Blanc, K., et al., Transplantation of mesenchymal stem cells to enhance engraftment of hematopoietic stem cells. Leukemia, 2007. 21(8): p. 1733-8. 78. Zappia, E., et al., Mesenchymal stem cells ameliorate experimental autoimmune encephalomyelitis inducing T-cell anergy. Blood, 2005. 106(5): p. 1755-61. 79. Gerdoni, E., et al., Mesenchymal stem cells effectively modulate pathogenic immune response in experimental autoimmune encephalomyelitis. Ann Neurol, 2007. 61(3): p. 219-27. 80. Zhang, J., et al., Human bone marrow stromal cell treatment improves neurological functional recovery in EAE mice. Exp Neurol, 2005. 195(1): p. 16-26. 81. Bai, L., et al., Human bone marrow-derived mesenchymal stem cells induce Th2-polarized immune response and promote endogenous repair in animal models of multiple sclerosis. Glia, 2009. 57(11): p. 1192-203. 82. Karussis, D., et al., Safety and immunological effects of mesenchymal stem cell transplantation in patients with multiple sclerosis and amyotrophic lateral sclerosis. Arch Neurol, 2010. 67(10): p. 1187-94. 83. Ma, Q., et al., Cell density plays a critical role in ex vivo expansion of T cells for adoptive immunotherapy. J Biomed Biotechnol, 2010. 2010: p. 386545. 84. Lan, Y.W., et al., Hypoxia-preconditioned mesenchymal stem cells attenuate bleomycin-induced pulmonary fibrosis. Stem Cell Res Ther, 2015. 6: p. 97. 85. English, K., et al., IFN-gamma and TNF-alpha differentially regulate immunomodulation by murine mesenchymal stem cells. Immunol Lett, 2007. 110(2): p. 91-100. 86. Fock, V., et al., Macrophage-derived IL-33 is a critical factor for placental growth. J Immunol, 2013. 191(7): p. 3734-43. 87. Murakami-Satsutani, N., et al., IL-33 promotes the induction and maintenance of Th2 immune responses by enhancing the function of OX40 ligand. Allergol Int, 2014. 63(3): p. 443-55. | |
dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/67066 | - |
dc.description.abstract | 自體免疫疾病是一種慢性發炎的疾病,且第一型輔助性T細胞與第十七型輔助性T細胞在其致病機轉中扮演不可或缺的角色。間質幹細胞具有免疫抑制的功能,並且被廣泛地研究作為許多自體免疫疾病療法的可能性。在本篇論文中,我們研究分離自新來源的胎盤絨毛膜褪膜間質幹細胞(pcMSC)是否具有抑制自體免疫疾病病人之T細胞功能的能力。我們也進一步探討pcMSC免疫調控能力的機轉,並研究IL-33是否在其中扮演一定的角色。我們發現pcMSC無法抑制小兒自體免疫疾病病人之T細胞。重要的是,pcMSC可以顯著地抑制多發性硬化症與視神經脊髓炎病人之完全活化的T細胞,不過它也意外地對低度活化之T細胞表現免疫促進的效果。我們更進一步證明pcMSC的促進效果不須依靠細胞之間的接觸,且經IFN-前處理後亦無法避免此現象的發生。再者,pcMSC的抑制與促進能力皆與IL-33無關。總結來說,pcMSC具有治療多發性硬化症與視神經脊髓炎的潛能,但其免疫促進的效果必須被審慎評估。 | zh_TW |
dc.description.abstract | Autoimmune disease is a type of chronic inflammatory disease, and T helper 1 (Th1) and T helper 17 (Th17) cells play a crucial role in its pathogenesis. Mesenchymal stem cells (MSC) possess immunosuppressive function and are widely studied as a potential cell therapy to many autoimmune diseases. Here, we investigated the therapeutic potential of the newly isolated placenta choriodecidual membrane-derived MSCs (pcMSCs) on T cell function of various autoimmune diseases. We also investigated the mechanisms of the immune-modulatory effects of pcMSCs, and evaluated whether IL-33 plays a role in them. We found that pcMSCs could not inhibit the T cells derived from pediatric autoimmune patients. Of note, pcMSCs significantly suppressed high-reactive T cells from adult multiple sclerosis (MS) and neuromyelitis optica (NMO) patients, although they displayed an unexpected enhancing effect on low-reactive T cells. We further demonstrated that the enhancing effect of pcMSCs is not dependent of cell-cell contact, and may not be prevented by IFN- pretreatment. Also, the suppressive and promoting function of pcMSCs were not mediated by IL-33. In conclusion, pcMSCs may have the potential to remedy MS and NMO, but their immune-enhancing effect should be carefully considered beforehand. | en |
dc.description.provenance | Made available in DSpace on 2021-06-17T01:18:56Z (GMT). No. of bitstreams: 1 ntu-106-R04424002-1.pdf: 1296252 bytes, checksum: 903ad07184e5a7a4d8cec67f4195d233 (MD5) Previous issue date: 2017 | en |
dc.description.tableofcontents | 致謝 i
中文摘要 ii Abstract iii Contents iv Chapter 1 Introduction 1 1.1 Autoimmune disease 2 1.2 Mesenchymal stem cells (MSCs) 4 1.2.1 The immunomodulatory property of MSCs 4 1.2.2 The interactions between MSCs and T cells 5 1.2.3 The immune-promoting ability of MSCs 6 1.2.4 The therapeutic role of MSCs in autoimmune diseases 7 1.2.5 Placenta choriodecidual membrane-derived mesenchymal stem cells (pcMSCs) 7 1.3 IL-33 8 1.4 Specific Aims 9 Chapter 2 Materials and Methods 10 2.1 Patients 11 2.2 Human peripheral blood mononuclear cells (PBMCs) separation 11 2.3 Proliferation assay 11 2.4 Cytokine secretion assay 12 2.5 T cells with suboptimal activation 12 2.6 Flow Cytometry Analysis 12 2.7 Enzyme-linked immunosorbent assay (ELISA) 13 2.8 RNA extraction 13 2.9 RT-qPCR 14 2.10 siRNA mediated IL-33 knockdown 14 2.11 Statistical analysis 14 Chapter 3 Results 16 3.1 pcMSCs suppress proliferation, activation and IFN-γ production of T cells in healthy donors. 17 3.2 The immunomodulatory effects of pcMSCs on T cells in pediatric patients with autoimmune diseases. 17 3.3 The double-edged immunomodulatory effects of pcMSCs on T cells in adult patients with neurologic autoimmune disease. 18 3.4 pcMSCs had immune-enhancing effects on low-reactive T cells. 18 3.5 pcMSCs did not have immune-enhancing effects on nonreactive T cells. 19 3.6 The contribution of cell-cell contact to the immune-enhancing capability of pcMSCs. 19 3.7 The effect of conditioned medium from high-reactive T cells on the immuno-enhancing capability of pcMSCs. 20 3.8 The effect of IFN-γ and TNF-α pretreatment on the immunomodulatory capability of pcMSCs. 20 3.9 IL-33 knockdown did not affect the immunosuppressive phenotype of pcMSCs on T cells. 21 Chapter 4 Discussion 23 Figures 29 Figure 1. pcMSCs suppress proliferation, activation and IFN-γ production of T cells in healthy donors. 30 Figure 2. The immunomodulatory effects of pcMSCs on T cells in pediatric patients with autoimmune diseases. 31 Figure 3. The double-edged immunomodulatory effects of pcMSCs on T cells in patients with neurologic autoimmune disease. 33 Figure 4. The immunomodulatory effects of pcMSCs on the frequency of IFN-γ producing T cells. 34 Figure 5. pcMSCs had immune-enhancing effects on low-reactive T cells. 36 Figure 6. pcMSCs did not have immune-enhancing effects on nonreactive T cells. 37 Figure 7. The contribution of cell-cell contact to the immune-enhancing capability of pcMSCs. 38 Figure 8. The effect of conditioned medium from high-reactive T cells on the immuno-enhancing capability of pcMSCs. 39 Figure 9. The effect of IFN-γ and TNF-α pretreatment on the immunomodulatory capability of pcMSCs. 41 Figure 10. pcMSCs express IL33. 42 Figure 11. IL-33 knockdown did not affect the expression of potential immunosuppressive mediators in pcMSCs. 43 Figure 12. IL-33 knockdown did not affect the immunomodulatory phenotype of pcMSCs on T cells. 45 Table 46 Table 1. The immunomodulatory effects of pcMSCs on T cells in patients with pediatric autoimmune disease. 47 Chapter 5 References 48 | |
dc.language.iso | en | |
dc.title | 探討間質幹細胞對自體免疫疾病病人之T細胞的免疫調控能力及其機制 | zh_TW |
dc.title | Study on the Immunoregulatory Effect of Mesenchymal Stem Cells on T Cells From Patients with Autoimmune Diseases and Its Mechanism | en |
dc.type | Thesis | |
dc.date.schoolyear | 105-2 | |
dc.description.degree | 碩士 | |
dc.contributor.oralexamcommittee | 周秀慧,孫昭玲,林泰元,胡忠怡 | |
dc.subject.keyword | 自體免疫疾病,間質幹細胞,T細胞,免疫調節,IL-33, | zh_TW |
dc.subject.keyword | autoimmune disease,mesenchymal stem cells (MSCs),T cells,immunomodulation,IL-33, | en |
dc.relation.page | 56 | |
dc.identifier.doi | 10.6342/NTU201702381 | |
dc.rights.note | 有償授權 | |
dc.date.accepted | 2017-08-12 | |
dc.contributor.author-college | 醫學院 | zh_TW |
dc.contributor.author-dept | 醫學檢驗暨生物技術學研究所 | zh_TW |
顯示於系所單位: | 醫學檢驗暨生物技術學系 |
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