Ford Focus 1.5 L ti 的問題，透過圖書和論文來找解法和答案更準確安心。 我們找到下列各種有用的問答集和懶人包

腫瘤浸潤淋巴細胞與腫瘤相關巨噬細胞/微膠細胞對腦瘤的調節機制

為了解決Ford Focus 1.5 L ti 的問題，作者巫鈺茹 這樣論述：

指導教授推薦書......................................................口試委員審定書......................................................序言與致謝..........................................................iii中文摘要..............................................................v英文摘要........................................

....................viiTABLE OF CONTENTS...................................ixORIGINAL PAPERS.....................................................xiiLIST OF FIGURES....................................................xiiiLIST OF TABLES......................................................xviLIST OF AB

BREVIATIONS.............................................CHAPTER I.............................................................1INTROCUCTION.......................................................11.1 Glioma classification and grading..............................11.2 Resistance in glioma.............

..............................21.3 Tumor-infiltrating lymphocytes (TILs)..........................81.4 The role of gioma-associated microglia/macrophages (GAMs).....101.5 The role of CCL5/CCL5 axis in GAMs............................131.6 Matrix metallopeptidase in glioma development ...............

.131.7 Objectives....................................................141.7.1 Hypothesis 1: an increase of CD38+HLA-DR+CD8+ TILs alongwith CCR5 level should have some reasons and functions inresponse to the presence of glioma.............................191.7.2 Hypothesis 2: the substantial amounts o

f GAMs should havesome reasons and functions in response to the presence of glioma...............................................................22CHAPTER II...........................................................25MATERIALS AND METHODS.............................................252.1 Standard p

rotocol approval, registration, and patient consent.252.2 Glioma cell culture...........................................252.3 Preparation of blood and tumor samples........................252.4 Multiparameter flow cytometry analysis........................262.5 Intracellular cytokine production assa

ys......................272.6 Immunohistocytology...........................................282.7 Quantitative real-time PCR....................................292.8 Western blotting..............................................302.9 Patient criteria, characteristics, histopathologicalverification a

nd specimen processing..............................302.10 Preparation of Glioma-Associated Macrophages/Microglia (GAMs)and CD8+ T cells from Patient Samples............................ 362.11 Retrospective analysis of CCL5 gene expression in humanglioma..............................................

..............382.12 Preparation of GAM-Conditioned Medium (GAM-CM) and CD8+ T-cellconditioned medium................................................382.13 Cytokine protein array.......................................382.14 Migration and invasion assays................................392.15 Zymograp

hy analysis..........................................392.16 Intracellular calcium assay..................................402.17 siRNA transfection...........................................402.18 ELISA........................................................402.19 Statistical analysis................

.........................40CHAPTER III .........................................................41RESULTS..............................................................413.1 Patients with glioma display a decrement of peripheral CD3+ Tcells in comparison to healthy donors.............................

413.2 Increased CD38+HLA-DR+CD8+ T cells and accumulation in the tumormicroenvironment in high-grade gliomas............................443.3 The concurrent expression of CCR5 and TNFR2 on CD38+HLA-DR+CD8+T cells from patient PBMCs and tumors.............................483.4 CD38+HLA-DR+CD8+ T cell

s from patient PBMCs produce IFN-γ andIL-2 upon stimulation with PMA and ION ...........................493.5 CCL5 and CD38+HLA-DR+CD8+ T-cell presentation in patient tumortissues ..........................................................533.6 Co-expression of functional and exhausted molecules inCC

R5+CD38+HLA-DR+CD8+ T cells in response to glioma...............573.7 CCL5 level, tumor volume and survival in glioma patients......603.8 CCL5 promotes heterogeneous glioma migration and invasion.....643.9 CCL5 induces PYK2 phosphorylation and MMP-2 activation........663.10 Controlling calcium level

s eliminates CCL5-regulated calcium-dependent protein kinases in glioma...............................683.11 Inhibition of CaMKII phosphorylation suppresses CCL5-inducedMMP-2 expression .................................................723.12 Inhibition of calcium-dependent signaling reduces GM-CM-in

ducedMMP-2 expression in glioma cells..................................75CHAPTER IV ..........................................................80DISCUSSION…......................................................80CHAPTER V ...........................................................88CONCLUSIONS, FUTUR

E WORK AND CHALLNGES............................88REFERENCES....................................................... 91LIST OF FIGURESFigure 1.1 Overview of the immune response and major immune checkpoint molecules in theimmune cycle of glioblastoma………………………………………………………….………….....2Figure 1.2 Immunoth

erapy-resistance classification scheme based on relative intrinsic and adaptiveresistance mechanisms………………………………………………..............................................…4Figure 1.3 Representative flowcytometric analysis…………………………………………..….......9Figure 1.4 Tumor progression followed by MRI……………………………………

……….….…..10Figure 1.5 The presence of glioma-associated microglia/macrophages………………………….…12Figure 1.6 The percentage expression CD4+and CD8+ T cells in healthy donors andpatients……………………………………………………………………..…….........................….15Figure 1.7 The percentage expression of FOX3P+CD4+ T cells were

lower in both newly andrecurrent patients’ PBMCs………………………………………….…………………………….....16Figure 1.8 Increased activation of CCR5 and TNFR2 in patient CD38+HLA-DR+CD8+TILs…………………………………………………………...………………………………...…..17Figure 1.9 Representative images of CD11b+CD45+/CD11b+CD45-(GAMs) expressed in low-gradean

d high-grade gliomas………………………………………….……………………………….….18Figure 2.1 (A-F) Representative H&E stains of tumor margin and glioma taken from newlydiagnosed glioma patients…………………………………………………..……………….…..….34Figure 2.2 (A) Representative images of CD11b+CD45+/CD11b+CD45-(GAMs) expressed in low-grade and hig

h-grade gliomas……………………………....……37Figure 3.1 Patients with glioma display a stepwise immune deficiency in accordance with the gradeclassification……………………………………………………...………………………………....44Figure 3.2 Pronounced activation and penetration of CD38+HLA-DR+CD8+ T cells in high-gradeglioma………………………………………………

…………………………………………….…46Figure 3.3 Increased activation of CCR5 and TNFR2 on CD38+HLA-DR+CD8+TILs…………………………………………………………………………………………….…...49Figure 3.4 IFN-γ and IL-2 production by CD38+HLA-DR+CD8+ T cells from patients with glioma isenhanced……………………………..…………………………………………………………..….52Figure 3.5 The associa

tion of CD38+HLA-DR+CD8+ T cell penetration and CCL5 expression inGBM……………………………………….………………………………………………….…….55Figure 3.6 CD8+ T cells of newly-diagnosed (n = 3) and recurrent (n = 3) patients enforce gliomaPD-L1 expression………………………..……………………………………………………….…56Figure 3.7 Co-expression of functional and

exhausted molecules in CCR5+CD38+HLA-DR+CD8+ Tcells in response to glioma…...…………………………………………………………….……….58Figure 3.8 Survival analysis results for CCL5 in newly diagnosed glioma patients. (A) CCL5expression quantified from four newly diagnosed GBM tissues……...……………………………61Figure 3.9 CCL5 promotes

human glioma migration………………………………….…….…….65Figure. 3.10 CCL5 promotes heterogeneous glioma invasive activity………………………....….66Figure. 3.11 CCL5 induces PYK2 phosphorylation and MMP-2 activation in gliomacells…………………………………………………………………………….........................……67Figure. 3.12 CCL5 induces a calciu

m-dependent signaling pathway in a concentration- and timedependent manner in glioma cells…………………...……………………………………………...69Figure 3.13 Immunocytochemistry stains of p-CaMKII protein expression in A172, U87, and W802cells after 24 h of CCL5 treatment………………………...………………………………………..71Figure. 3.14 Inhibiti

on of CaMKII phosphorylation downregulates CCL5-induced MMP-2expression…………………………………………………………………………………………...73Figure. 3.15 The increased MMP-2 expression by GM-CM is suppressed by inhibition of calciumrelated signaling pathways……………………………………………………………………….....77Figure 3.16 Three representative images

of isolated CD8+ T cells….........................……………..79Figure 5.1 Schematic diagram …..........................................................……………………………89LIST OF TABLESTable 1.1 Molecular classification of GBM………………………………………….……..….…….5Table 2.1 The clinical information of newly diagnosed gli

oma patients enrolled in survivalanalysis…………………………………………………………………......................................….32Table 2.2 Patient characteristics for prospective study………………………………………....…..33Table 3.1 Study population of healthy donors and patients with glioma……………………….......42Table 3.2 Descriptive stat

istics of the study population and mean age difference………………....42Table 3.3 Results of Independent t test for age differences between healthy donor and patientgroups…………………………………………………………………………………………….....43Table 3.4 Univariate and multivariate Cox regression analysis of glioma prognostic factorsaff

ecting survival rate…………………………………………………………………………..…...63