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  1. NTU Theses and Dissertations Repository
  2. 醫學院
  3. 臨床醫學研究所
Please use this identifier to cite or link to this item: http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/39324
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dc.contributor.advisor黃思誠(Su-Cheng Huang),江伯倫,許博欽(Bor-Ching Sheu)
dc.contributor.authorWen-Chun Changen
dc.contributor.author張文君zh_TW
dc.date.accessioned2021-06-13T17:26:03Z-
dc.date.available2007-01-28
dc.date.copyright2005-01-28
dc.date.issued2005
dc.date.submitted2005-01-20
dc.identifier.citationAsselin-Paturel C, Echchakir H, Carayol G, et al. Quantitative analysis of Th1, Th2 and TGF-beta1 cytokine expression in tumor, TIL and PBL of non-small cell lung cancer patients. Int J Cancer 1998;77:7-12.
Armstrong B., and Doll R. Environmental factors and cancer incidence and mortality in different countries, with special reference to dietary practices. Int J Cancer 1975;15:617-31.
Atkinson EA, et al. Cytotoxic T lymphocyte-assisted suicide. Capase 3 activation is primarily the result of the direct action of granzyme B. J Biol Chem 1998;273:21261-6.
Bakker ABH, Philips JH, Figdor CG, et al. Killer cell inhibitory receptors for MHC class I molecules regulate lysis of melanoma cells mediated by NK cells, γδ T cells, and antigen-specific CTL. J Immunol 1998;160:5239-45.
Bergstrom A, Pisani P, Tenet V, et al. Overweight as an avoidable cause of cancer in Europe. Int J Cancer 2001;91: 421-30.
Bertone S, Schiavetti F, Bellomo R, et al. Transforming growth factor-β-induced expression of CD94/NKG2A inhibitory receptors in human T lymphocytes. Eur J Immunol 1999;29:23-9.
Birkeland SA. et al. Cancer risk after renal transplant in the Nordic countries, 1964-1986. Int J Cancer 1995;60:183-9.
Borrego F., UlbrechtM, Weiss EH, et al. Recognition of human histocompatibility leukocyte antigen (HLA) –E complex with HLA class I signal sequence-derived peptide by CD94/NKG2 confers protection from natural killer cell-mediated lysis. J Exp Med 1998;187:813-8.
Boshoff C. and Weiss R. AIDS-related malignancies. Nature Rev Cancer 2002;2:373-82.
Briard D, Boyé DB, Azzarone B, et al. Fibroblasts from human spleen regulate NK cell differentiation from blood CD34+ progenitors via cell surface IL-15. J Immunol 2002;168:4326-32.
Chang HL, Gillett N, Figari I, et al. Increased transforming growth factor β expression inhibits cell proliferation in vitro, yet increases tumorigenecity and tumor growth of Meth A carcinoma cells. Cancer Res 1993;53:4391-8.
Chien YH, Davis MM. How alpha beta T-cell receptors 'see' peptide MHC complexes. Immunol Today 1993;14:597-602.
Chouaib S, Asselin-Paturel C, Mami-Chouaib F, et al. The host-tumor immune conflict. Immunol Today 1997;18:493-7.
Clemente CG, et al. Prognostic value of tumor infiltrating lymphocytes in the vertical phase of primary cutaneous melanoma. Cancer 1996;77:1303-10.
Coleman MP, Esteve J, Damiecki P, et al. Trends in Cancer Incidence and Mortality. IARC Sci. Publ., 1-806. Lyon, France: International Agency for Research on Cancer, 1993.
Derre L, Corvaisier M, Pandolfino MC, et al. Expression of CD94/NKG2-A on human T lymphocytes is induced by IL-12: Implications for adoptive immunotherapy. J Immunol 2002;168:4864-70.
Dunn JE. Cancer epidemiology in populations of the United States-with emphasis on Hawaii and California and Japan. Cancer Res 1975;35: 3240-5.
Ebert EC, Roberts AI, Devereux D, et al. Selective immunosuppressive action of a factor produced by colon cancer cells. Cancer Res 1990;50:6158.
Ehrlich P. Ueber den jetzigen stand der Karzinomforschung. Ned Tijdschr Geneeskd 1909;5:273-90.
Epstein NA. and Fatti LP. Prognostic carcinoma: some morphological features affecting prognosis. Cancer 1976;37:2455-65.
Gati A, Guerra N, Giron-Michel J, et al. Tumor cells regulate the lytic activity of tumor-specific cytotoxic T lymphocytes by modulating the inhibitory natural killer receptor function. Cancer Res 2001;61:3240-4.
Guerra N, Guillard M, Angevin E, et al. Killer inhibitory receptor (CD158b) modulates the lytic activity of tumor-specific T lymphocytes infiltrating renal cell carcinomas. Blood 2000;95:2883-9.
Herberman RB. Cellular immunity. The molecular basis of cancer. 1995;511-21.
Hill HA, and Austin H. Nutrition and endometrial cancer. Cancer Causes Control 1996;7:19-32.
Ikeda H, Lethe B, Lehmann F, et al. Characterization of an antigen that is recognized on a melanoma showing partial HLA loss by CTL expressing an NK inhibitory receptor. Immunity 1997;6:199-208.
Jass JR. Lymphocytic infiltration and survival in rectal cancer. J Clin Pathol 1986;39:585-9.
Jemal A, Thomas A, Murray T, et al. Cancer statistics, 2002. CA Cancer J Clin 2002;52:23-47.
Kaaks R, Lukanova A and Kurzer MS. Obesity, endogenous hormones, and endometrial cancer risk: A synthetic review. Cancer Epidemiology, Biomarkers & Prevention, 2002; 11:1531-43.
Kim J, Modlin RL, Moy RL, et al. IL-10 production in cutaneous basal and squamous cell carcinomas- A mechanism for evading the local T cell immune response. J Immunol;1995:155: 2240-7.
Lanier LL. NK cell receptors. Ann Rev Immunol 1998;16:359-93.
Lin Z, Conejo-Garcia JR, Katsaros D, et al. Intratumoral T cells, recurrence, and survival in epithelial ovarian cancer. N Engl J Med 2003;348:203-13.
Lipponen PK, Eskelinen MJ, Jauhianen K, et al. Tumor infiltrating lymphocytes as a independent prognostic factor in transitional cell bladder cancer. Eur J Cancer 1992;29A:69-75.
Liu L, Chahroudi A, Silvestri G, et al. Visualization and quantification of T cell-mediated cytotoxicity using cell-permeable fluorogenic capase substrates. Nature Med 2002;8:185-9.
Lu J, Giuntoli RL II, , Omiya R, et al. Interleukin 15 promotes antigen-independent in vitro expansion and long-term survival of antitumor cytotoxic T lymphocytes. Clin Cancer Res 2002;8:3877-84.
Lurain JR. Uterine cancer. In: Johnathan S. Bebrek (eds) Novak's Gynecology. Lippincott Williams & Wilkins, Philadelphia, 2002, pp 1143.
Lyngstrand ST, Würtzen PA, Ødum N, et al. IL-15 induces unspecific effector functions in human peptide-specific CD8+ T cell- cultures. Scand J Immunol 2002;56:602-10.
Mingari MC, Schiavetti F, Ponte M, et al. Human CD8+ T lymphocyte subsets that express HLA class I–specific inhibitory receptors represent oligoclonally or monoclonally expanded cell populations. Proc Natl Acad Sci USA 1996;93:2433-8.
Mingari MC, Ponte M, Bertone S, et al. HLA class I-specific inhibitory receptors in human T lymphocytes: Interleukin 15-induced expression of CD94/NKG2A in superantigen- or alloantigen-activated CD8+ T cells. Proc Natl Acad Sci USA 1998a;95:1172-7.
Mingari MC, Moretta A, Moretta L. Regulation of KIR expression in human T cells: a safety mechanism that may impair protective T-cell responses. Immunol Today. 1998b;19:153-7.
Moretta A, Vitale M, Bottino C, et al. P58 molecules as putative receptors for MHC class I molecules in human natural killer (NK) cells. Anti-p58 antibodies reconstitute lysis of MHC class I-protected cells in NK clones displaying different specificities. J Exp Med 1993;178:597-604.
Moretta A, Biassoni R, Bottino C, et al. Major histocompatibility complex class I–specific receptors on human natural killer and T lymphocytes. Immunol Rev 1997;155:105-17.
Moy PM, Holmes EC, and Golub SH. Depression of natural killer cytotoxic activity in lymphocytes infiltrating human pulmonary tumors. Cancer Res 1985;45:57-60.
Naito Y, et al. CD8+ T cells infiltrated whitin cancer cell nests as a prognostic factor in human colorectal cancer. Cancer Res 1998:58:3491-4.
Old LJ. and Boyse EA. Immunology of experimental tumors. Annu Rev Med 1964;15:167-86.
O’Mahony AM, O’Sullivan GC, O’Connell J, et al. An immune suppressive factor derived from esophageal squamous carcinoma induces apoptosis in normal and transformed cells of lymphoid lineage. J Immunol 1993;151:4847-56.
Palma L., Di Lorenzo N., Guidetti B. Lymphocytic infiltrates in primary glioblastoma and recidivous gliomas. Incidence, fate and revalence to prognosis in 228 operated cases. J Neuosurg 1978;49:854-61.
Parker SL, Tong T, Bolden S, et al. Cancer statistics, 1997. CA 1997;47:5-27.
Parkin S, Whelan L, Ferlay J, et al. (eds.), Cancer incidence in five continents. In: D. M.IARC Scientific. Publication. No. 143, Vol. VII, pp. 1-1240. Lyon, France: International Agency for Research on Cancer, 1997.
Pende D, Biassoni R, Cantoni C, et al. The natural killer cell receptor specific for HLA-A allotypes: a novel member of the p58/p70 family of inhibitory receptors that is characterized by three immunoglobulin-like domains and is expressed as a 140 kD disulphide-linked dimer. J Exp Med 1996;184:505-18.
Pende D, Accame L, Pereti L, et al. The susceptibility to natural killer cell-mediated lysis of HLA class I-positive melanomas reflects the expression of insufficient amounts of different HLA class I alleles. Eur J Immunol 1998;28:2384.
Penn I. Malignant tumors in Organ transplant recipients (Springer-Verlag, New York, 1970)
Penn I. Posttransplant malignancies. Trasplant Proc 1999;31:1260-2.
Ranges GE, Figari IS, Espevik T, et al. Inhibition of cytotoxic T cell development by transforming growth factor beta and reversal by recombinant tumor necrosis factor alpha. J Exp Med 1987;166:991-8.
Rilke F, et al. Prognostic significance of HER-2/neu expression in breast cancer and its relationship to other prognostic factors. Int J Cancer 1991;49:44-9.
Sheu BC, Lin RH, Ho HH, et al. Down-regulation of CD25 expression on activated tumor-infiltrating lymphocytes derived from human cervical carcinoma. Human Immunol 1997;56:39-48.
Sheu BC, Hsu SM, Ho HN, et al. Tumor immunology- When a cancer cell meets the immune cells. J Formos Med Assoc 1999:98:730-5.
Sheu BC, Lin RH, Lien HC, et al. Predominant Th2/Tc2 polarity of tumor-infiltrating lymphocytes in human cervical cancer. J Immunol 2001;167:2972-8.
Sheu, BC, Hsu SM, Ho HN, et al. A novel role of metalloproteinase in cancer-mediated immunosuppression. Cancer Res. 2001;61:237.
Sheu BC, Lien HC, Ho HN, et al. Increased expression and activation of gelatinolytic matrix metalloproteinases is associated with the progression and recurrence of human cervical cancer. Cancer Res 2003;63:6537-42.
Sindhu ST, Ahmad R, Morisset R, et al. Peripheral blood cytotoxic gammadelta T lymphocytes from patients with human immunodeficiency virus type 1 infection and AIDS lyse uninfected CD4+ T cells, and their cytocidal potential correlates with viral load. J Virol 2003;77:1848-55.
Speiser DE, Pittet MJ, Valmori D, et al. In vivo expression of natural killer-cell inhibitory receptors by human melanoma-specific cytolytic T lymphocytes. J Exp Med 1999;190:775-82.
Stutman O. Immunodepression and malignancy. Adv Cancer Res 1975;22:261-422.
Sulitzeanu D. Immunosuppressive factors in human cancer. Adv Cancer Res 1993:60;247.
Tanaka J, Toubai T, Tsutsumi Y, et al. Cytolytic activity and regulatory functions of inhibitory NK cell receptor–expressing T cells expanded from granulocyte colony-stimulating factor–mobilized peripheral blood mononuclear cells. Blood 2004;104:768-74.
Parekh TV, Gama P, Wen X, et al. Transforming growth factor-β signaling is disabled early in human endometrial carcinogenesis concomitant with loss of growth inhibition. Cancer Res 2002;62:2778-90.
Vitale M, Sivori S, Pende D, et al. Physical and functional independency of p70 and p58 cell receptors for HLA class I: Their role in the definition of different groups of alloreactive NK cell clones. Proc Natl Acad Sci USA 1996;93:1453-7.
Vose BM and Moore M. Human tumor-infiltrating lymphocytes: a marker of host response. Semin Hematol 1985;22:27-40.
Voorzanger N, Touitou R, Garcia E, et al. Interleukin (IL)-10 and IL-6 are produced in vivo by non-Hodgkin’s lymphoma cells and act as cooperative growth factors. Cancer Res 1996;56:5499-505.
Whiteside TL, Jost LM, Herberman RB. Tumor-infiltrating lymphocytes: potential and limitation of their use for cancer therapy. Crit Rev Oncol Hematol 1992;12:25-47.
dc.identifier.urihttp://tdr.lib.ntu.edu.tw/jspui/handle/123456789/39324-
dc.description.abstract背景與目的
子宮内膜癌在美國是女性生殖系統最常見的侵襲癌,自1950年以來,雖然子宮内膜癌的死亡率降低超過 60%,其發生率卻明顯增加,而且年齡層有逐漸降低的趨勢。我們知道腫瘤細胞在癌化過程中,一方面需要大量繁殖增生,另一方面則需對抗來自宿主體內免疫系統的清除作用,才能達到其侵入深部組織與蔓延的目的。因此雖然在腫瘤組織發現有大量的腫瘤內浸潤淋巴球 (tumor infiltrating lymphocytes,TILs),許多免疫逃避性機轉仍被提出,說明這些腫瘤內浸潤淋巴球對抗腫瘤的毒殺能力微弱,自然殺手細胞 (natural killer cells,NK cells) 活性低,且對於腫瘤刺激的增生反應能力小。有人發現自然殺手細胞抑制受體 (inhibitory natural killer cell receptors,iNKRs),存在於自然殺手細胞及 T 細胞,可抑制自然殺手細胞的活性與 CD8+ T 細胞的毒殺能力。我們的研究目的在於找出子宮内膜癌細胞逃避宿主的免疫監控與自然殺手細胞抑制受體之相關性,進一步希望對於未來發展免疫調節治療有所幫助。
材料與方法
我們利用機械式研磨萃取法 (mechanical dispersal technique) 來獲得子宮内膜癌之腫瘤內浸潤淋巴球,進一步利用細胞免疫螢光染色及流體細胞儀分析子宮内膜癌腫瘤中浸潤淋巴球表面自然殺手細胞抑制受體的分布。
結果
我們在子宮内膜癌組織分離出的單核細胞球相對於正常子宮内膜組織中有較多的現象 (8450/5655),且子宮内膜癌病患分離出的腫瘤內浸潤 CD3+ T 淋巴球比正常子宮内膜病患分離出的正常子宮内膜浸潤 CD3+ T 淋巴球有較高表現比例 (子宮内膜癌90.05%; 正常子宮内膜79.60,P = 0.086),表示子宮内膜癌組織可能比正常子宮内膜組織含有更多的浸潤淋巴球,因此 CD3+ T 淋巴球對於子宮内膜癌之抗癌免疫反應可能扮演重要角色。在進一步的研究當中,發現從子宮内膜癌組織分離出來的浸潤 CD3+ CD8+ T 淋巴球顯著比週邊血液 CD3+ CD8+ T 淋巴球含有較高表現比例的CD94 及 NKG2A,流體細胞儀分析顯示8.40%的子宮内膜癌浸潤淋巴球表現 CD94 (子宮内膜癌,8.40% [4.95-13.73];週邊血液,3.80% [1.30-5.00],P = 0.013),而15.90%的子宮内膜癌浸潤淋巴球表現 NKG2A (子宮内膜癌,15.90% [8.25-21.15],週邊血液,2.10% [1.15-5.30],P < 0.001);CD94 及 NKG2A 的表現比例在子宮内膜癌浸潤淋巴球顯著高於控制組的週邊血液單核細胞球及正常子宮内膜組織,這些現象暗示著腫瘤可能分泌某種物質,以改變自然殺手細胞抑制受體在 T 細胞上的表現,而高度表現於子宮内膜癌組織浸潤淋巴球的自然殺手細胞抑制受體,可能會抑制淋巴球的毒殺反應,並且使其失去對腫瘤的局部免疫控制。除此之外,我們也觀察到 CD158b 及 NKB1 高度表現於子宮内膜癌病患的週邊血液 CD3+ CD8+ T 淋巴球 (CD158b:子宮内膜癌組織,3.80% [1.08-7.28];週邊血液,10.70% [4.95-14.98],P = 0.001;NKB1:子宮内膜癌組織,0.40% [0.00-0.80];週邊血液,2.20% [0.43-3.88],P = 0.045),而這些現象可能會使全身免疫系統對於腫瘤的控制降低。
我們第二部分的研究,主要為利用流體細胞儀 PhiPhiLux 毒殺試驗分析高度表現於 CD3+ CD8+ T 淋巴球上的 CD94/NKG2A 對於其毒殺能力的影響。結果顯示CD94/ NKG2A 在 CD3+ CD8+ T 淋巴球上的高度表現明顯會降低其毒殺能力,而阻斷了 CD94 或 NKG2A 與 HLA class I 分子的作用,則可增加其毒殺能力,NKG2A的阻斷對於 CD3+ CD8+ T 淋巴球的毒殺能力的增加明顯高於 CD94 的阻斷,且愈高的 E/T ratio 差別愈明顯。所以高度表現於 CD3+ CD8+ T 淋巴球上的 CD94 或 NKG2A 可能與其無法有效毒殺子宮内膜癌細胞有關。
結論
由於人類子宮内膜癌腫瘤細胞可產生大量之細胞激素 (cytokines),而免疫細胞表面自然殺手細胞抑制受體可能受細胞激素之影響,進一步抑制了免疫細胞對於子宮内膜癌的抗癌反應。因此,子宮内膜癌細胞本身可能提供必要的訊息,使對抗腫瘤的專一毒殺性淋巴球表現出自然殺手細胞抑制受體,使子宮内膜癌逃過免疫監控。我們期待在不久的將來,可釐清高度表現於子宮内膜癌組織浸潤淋巴球的自然殺手細胞抑制受體在活體內 (in vivo) 上的功能,與其對於子宮内膜癌細胞免疫監控的影響,更進一步幫助我們對於未來抗癌藥物的發展。
zh_TW
dc.description.abstractBackground: To investigate the expression of inhibitory natural killer receptors (iNKRs) within the human tumor milieu, we directly examined the in vivo expressions of various iNKRs on tumor-infiltrating lymphocytes (TILs) derived from human endometrial carcinoma (EC).
Material and Methods: Totally 22 patients with Stage Ia–IIIa EC were enrolled. TILs were isolated from tissue specimens by means of a mechanical dispersal technique. The subpopulations of immunocytes were quantified and expressions of NKRs on CD8
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dc.description.tableofcontents目錄
一、中文摘要•••••••••••••••••••••••••••••••••••••••1
二、緒論
研究背景•••••••••••••••••••••••••••••••••••••••••••3
子宮内膜癌的發生率••••••••••••••••••••••••••••••••••3
免疫監督與腫瘤內浸潤淋巴球••••••••••••••••••••••••••••3
免疫逃避性••••••••••••••••••••••••••••••••••••••••••4
自然殺手細胞抑制受體•••••••••••••••••••••••••••••••••4
細胞激素與自然殺手細胞抑制受體•••••••••••••••••••••••••6
研究目的••••••••••••••••••••••••••••••••••••••••••••7
研究的假說••••••••••••••••••••••••••••••••••••••••••7
三、研究方法與材料
病例收集••••••••••••••••••••••••••••••••••••••••••••8
機械式研磨萃取•••••••••••••••••••••••••••••••••••••••8
流體細胞儀分析••••••••••••••••••••••••••••••••••••••8
表現比例的定義••••••••••••••••••••••••••••••••••••••9
細胞激素(rhIL-15)誘發CD94/NKG2A分析••••••••••••••••••••9
流體細胞儀細胞毒殺分析•••••••••••••••••••••••••••••••9
統計分析•••••••••••••••••••••••••••••••••••••9
四、結果
第一部分
子宮内膜癌組織及正常子宮内膜組織的重量及分離出的細胞•••••11
子宮内膜癌病患的週邊血液單核細胞球及腫瘤內浸潤淋巴球之比較-- CD3+ 腫瘤內浸潤淋巴球含有較高表現比例的 CD8+ T 淋巴球••11
子宮内膜癌病患的週邊血液單核細胞球分離出來的 CD3+ CD8+ T 淋巴球含有較高表現比例的CD158b及NKB1•••••••••••••••••••11
子宮内膜癌病患的腫瘤內浸潤淋巴球分離出來的 CD3+ CD8+ T 淋巴球含有較高比例的CD94/NKG2A•••••••••••••••••••••••••••12
第二部分
活體外 (in vitro) rhIL-15 刺激 CD3+ CD8+ T 淋巴球表現 CD94/NKG2A•••••••••••••••••••••••••••••••••••••••••12
rhIFN-γ可明顯誘導出 HLA class I 分子高度表現於 K562 標的細胞上•••••••••••••••••••••••••••••••••••••••••••••••12
CD94/NKG2A在 CD8+ T 淋巴球上的高度表現明顯會降低其毒殺能力••••••••••••••••••••••••••••••••••••••••••••••••12
五、討論••••••••••••••••••••••••••••••••••••••••••14
六、展望
子宮内膜癌組織內細胞激素之表現••••••••••••••••••••••17
腫瘤細胞與自體免疫細胞的混合培養分析••••••••••••••••••17
子宮内膜癌組織腫瘤內浸潤CD3+ CD8+ T 淋巴球之毒殺分析•••••18
七、論文英文簡述 (summary)
Abstract••••••••••••••••••••••••••••••••••••••••••19
Introduction•••••••••••••••••••••••••••••••••••••••20
Material and Methods••••••••••••••••••••••••••••••••22
Results•••••••••••••••••••••••••••••••••••••••••••27
Discussion••••••••••••••••••••••••••••••••••••••••31
八、參考文獻•••••••••••••••••••••••••••••••••••••••34
九、圖表••••••••••••••••••••••••••••••••••••••••••43

圖表目錄
圖一、自然殺手細胞抑制受體影響毒殺性 T 淋巴球毒殺力之機轉••••••••••••••••••••••••••••••••••••••••••••••••43
圖二、自然殺手細胞抑制受體影響毒殺性淋巴球對被病毒感染或腫瘤細胞之毒殺力的機轉••••••••••••••••••••••••••••44
圖三、流體細胞儀分析下相互比較由子宮内膜癌組織 (i-p) 或週邊血液單核細胞球 (a-h) 分離出之 CD3+ CD4+ 或 CD3+ CD8+ T 淋巴球上自然殺手細胞抑制受體 (CD158a, CD158b, 及NKB1) 的表現•45
圖四、流體細胞儀分析下相互比較CD94 及 NKG2A 於子宮内膜癌組織 (g-l) 與週邊血液單核細胞球 (a-f) 分離出之 CD3+ CD4+ 或 CD3+ CD8+ T 淋巴球上的表現•••••••••••••••••••••••••••46
圖五、活體外 (in vitro) rhIL-15 刺激 CD3+ CD8+ T 淋巴球表現 CD94••••••••••••••••••••••••••••v•••••••••••••47
圖六、活體外 (in vitro) rhIL-15 刺激 CD3+ CD8+ T 淋巴球表現 NKG2A••••••••••••••••••••••••••••••••••••••••••••••48
圖七、將 K562 細胞以 rhIFN-γ (200 ng/ml) 刺激活化2天,誘導出 HLA class I 分子的表現••••••••••••••••••••••••••••••••••••••••••••••••49
圖八、流體細胞儀分析在不同比例的效應細胞與標的細胞 (E/T ratio = 1:1,3:1,9:1) 下,PhiPhiLux 毒殺分析試驗的結果••••••••••••••••••••••••••••••••••••••••••••••50
圖九、比較在不同比例的效應細胞與標的細胞下5組毒殺分析試驗的結果•••••••••••••••••••••••••••••••••••••••••••••••51
表一、子宮内膜癌組織及正常子宮内膜組織的平均重量及分離出的細胞••••••••••••••••••••••••••••••••••••••••••••••••52
表二、子宮内膜癌病患與正常子宮内膜病患分離出的週邊血液單核細胞球及腫瘤或正常子宮内膜組織內浸潤淋巴球之比較•••••••53
表三、流體細胞儀分析比較子宮内膜癌病患與正常子宮内膜病患分離出的週邊血液單核細胞球及腫瘤或正常子宮内膜組織內浸潤淋巴球,其自然殺手細胞抑制受體 (CD158a, CD158b, NKB1, CD94, NKG2A) 於 CD8+ T 淋巴球之表現•••••••••••••••••••••••••54
dc.language.isozh-TW
dc.subject腫瘤內浸潤淋巴球zh_TW
dc.subject自然殺手細胞抑制受體zh_TW
dc.subject膜癌zh_TW
dc.subject子宮&#20869zh_TW
dc.subjectendometrial canceren
dc.subjectinhibitory natural killer receptorsen
dc.subjecttumor-infiltrating lymphocytesen
dc.title子宮內膜癌腫瘤內免疫細胞及抑制受體分析zh_TW
dc.titleAnalysis of Inhibitory Natural Killer Receptors on Tumor Infiltrating Lymphocytes Derived from Human Endometrial Canceren
dc.typeThesis
dc.date.schoolyear93-1
dc.description.degree碩士
dc.contributor.oralexamcommittee#VALUE!
dc.subject.keyword膜癌,自然殺手細胞抑制受體,腫瘤內浸潤淋巴球,子宮&#20869,zh_TW
dc.subject.keywordtumor-infiltrating lymphocytes,endometrial cancer,inhibitory natural killer receptors,en
dc.relation.page54
dc.rights.note有償授權
dc.date.accepted2005-01-21
dc.contributor.author-college醫學院zh_TW
dc.contributor.author-dept臨床醫學研究所zh_TW
Appears in Collections:臨床醫學研究所

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