Marincola / Wang Immunologic Signatures of Rejection

1. Auflage 2010
ISBN: 978-1-4419-7219-4
Verlag: Springer US
Format: PDF
Kopierschutz: 1 - PDF Watermark

E-Book, Englisch, 353 Seiten, eBook

This book discusses the mechanisms leading to immune-mediated tissue rejection following the hypothesis that independent of the disease process the final effector mechanism is shared by most (but not all) pathologies and it is relatively simple. The book covers evidence gathered to support the thesis by studies performed in humans during rejection or in experimental models and will focus particularly (but not exclusively) on the analysis of the rejected tissue rather than the systemic circulation. Several disease processes are discussed including example of chronic inflammatory process without resolution of the pathologic process and acute one with resolution of the pathologic process (clearance of pathogen, rejection of tumor) or unwanted tissue destruction (allograft rejection, autoimmunity).

Zielgruppe

Research

Autoren/Hrsg.

Wang, Ena

Marincola, Francesco M.

Inhaltsverzeichnis

1;Contents;6
2;Part I:Preamble;10
2.1;From the “Delayed Allergy Reaction” to the “Immunologic Constant of Rejection”;11
2.1.1;From the Delayed Allergy Reaction to the Immunologic Constant of Rejection;11
2.1.2;Interferon Regulatory Factor (IRF)-1: Master Switch of Inflammation;13
2.1.3;The Recurrent Themes Defining the Signatures of Rejection;13
2.1.4;References;14
3;Part II:The Immune Biology of Rejection:Basic Principles;17
3.1;The Yin Yang of Cancer RelatedInflammation;18
3.1.1;Introduction;18
3.1.2;Recruitment of TAM;19
3.1.3;Plasticity of TAM and Promotion of Metastasis;19
3.1.4;Protective Inflammation and Macrophage Activation;20
3.1.5;References;20
3.2;The Immune Rejection: Lessonsfrom Experimental Models;24
3.2.1;Introduction;24
3.2.2;Rejection of Intestinal Microbiota;25
3.2.3;Rejection of Acute Infections;26
3.2.4;Chronic Inflammation in Obesity;27
3.2.5;Tumor Rejection;28
3.2.6;Concluding Remarks;30
3.2.7;References;30
3.3;Turning on and off the Immunological Switch: Immune Response Polarization and Its Control by IL-10 and STAT3;33
3.3.1;T Helper Cell Lineages;33
3.3.2;Differentiation and Activation of T Helper Lineages;35
3.3.3;Function and Plasticity of Th and Treg Lineages In Vivo;36
3.3.4;IL-10 Controls Inflammation;37
3.3.5;Regulation of IL-10 Production;39
3.3.6;IL-10 Signaling and Role of STAT3 in its Regulatory Functions;40
3.3.7;IL-10 has Superior Anti-Inflammatory Activity Compared with Other STAT3-Signaling Cytokines: Role of SOCS3;42
3.3.8;Molecular Mechanisms of the IL-10-Mediated Anti-Inflammatory Effects;43
3.3.9;Roles of STAT3 in Health and Disease;46
3.3.10;Roles of STAT3 in Cancer;47
3.3.11;STAT3 and IL-10 in Cancer-Promoting Inflammation;48
3.3.12;IL-10 Inhibition Facilitates Immune Responses to Tumors;48
3.3.13;Targeting STAT3 Facilitates Anti-Tumor Immune Responses;50
3.3.14;Conclusions;54
3.3.15;References;54
3.4;The Angiogenic Switch: Role of Immune Cells;62
3.4.1;Introduction;62
3.4.2;Innate Immunity;64
3.4.2.1;Macrophages and the Macrophage Polarization Paradigm;64
3.4.2.2;Tumor Associated Macrophages (TAMs);65
3.4.2.3;Tie2 Expressing Macrophages;66
3.4.3;Myeloid Derived Suppressor Cells (MDSCS);67
3.4.4;Granulocytes;67
3.4.5;Mast Cells;69
3.4.6;Dendritic Cells;70
3.4.6.1;DCs and Angiogenesis;70
3.4.7;NK Cells;71
3.4.7.1;NK Localization;72
3.4.8;Specific Immunity;72
3.4.9;Conclusions;72
3.4.10;References;73
3.5;Chemokines and Cytotoxic Effector Molecules in Rejection;81
3.5.1;Chemokines;82
3.5.1.1;Translation to Clinical Utility;85
3.5.2;Cytotoxic Effector Molecules;88
3.5.3;Conclusion;90
3.5.4;References;91
3.6;Clinical Applications of Activated Immune Cells;97
3.6.1;Introduction;97
3.6.2;Immune Therapy for Viral Infections;97
3.6.2.1;Cytomegalovirus;97
3.6.3;Immune Therapy for Viral Induce Malignancies;98
3.6.3.1;Posttransplant EBV-Associated Lymphoproliferative Disease;98
3.6.4;Immune Therapy for Leukemia;99
3.6.4.1;Donor Leukocyte Infusions;99
3.6.4.2;NK Cells;99
3.6.5;Immune Therapy for Cancer;100
3.6.5.1;Tumor Infiltrating Leukocytes for Melanoma;100
3.6.5.2;Dendritic Cells;101
3.6.5.3;New Directions;104
3.6.6;References;104
4;Part III:Circulating Patterns Associated with Chronic and Acute Immune Pathology;107
4.1;Blood Transcriptional Fingerprints to Assess the Immune Status of Human Subjects;108
4.1.1;Blood Transcript Profiling;108
4.1.2;Profiling Human Subjects in Health and Disease;110
4.1.2.1;Profiling Autoimmune Diseases;110
4.1.2.2;Profiling Infectious Diseases;111
4.1.2.3;Profiling other Diseases;112
4.1.3;Technology Primer (Fig. 1);113
4.1.4;Microarray Data Analysis;114
4.1.4.1;Analysis Primer;115
4.1.4.2;Analysis of Significance Patterns;116
4.1.4.3;A Modular Analysis Framework;117
4.1.4.4;Interpretation;118
4.1.5;Conclusions;120
4.1.6;References;120
4.2;Innate Signatures of Immune Mediated Resolution and Persistence of Hepatitis C Virus Infections;129
4.2.1;HCV Disease and Therapy;130
4.2.2;Viral Clearance;130
4.2.3;HCV Viral Proteins Modulate the Innate Response;131
4.2.4;Acute HCV Infection and Intrahepatic Induction of ISGs;132
4.2.5;Chronic HCV Infection and Hepatic ISG Expression;134
4.2.6;IL28B (IFNl3) in HCV Viral Clearance and Response to Therapy;136
4.2.7;T Cell Response and Viral Clearance;137
4.2.8;Conclusions;139
4.2.9;References;139
4.3;Immune Signatures and Systems Biology of Vaccines;143
4.3.1;Vaccine Development;144
4.3.1.1;Immune Response;144
4.3.1.2;Vaccines;144
4.3.1.3;Innate Immunity and Vaccine Recognition;145
4.3.1.4;Innate Signaling and Translation to the AdaptiveImmune Response;146
4.3.1.5;Hitting Innate Immune System by Vaccines;148
4.3.1.6;TLRs Signaling for a Potent and Prolonged Adaptive Immune Responses;149
4.3.1.7;Vaccines Inducing Humoral or Cellular Immune Response;149
4.3.2;Platform of System Levels Analyses;151
4.3.2.1;Systems Biology in Vaccine Studies;151
4.3.2.2;Role of Transcriptomics;151
4.3.2.3;Proteomics;153
4.3.2.4;RNAi and miRNA to Study Innate Immunity;153
4.3.2.5;Genetic Polymorphisms in Innate Immunity Genes;154
4.3.2.6;Systems Biology for Prediction of Vaccine Immunogenicity;154
4.3.2.6.1;Gene Signatures of Yellow Fever Vaccine YF-17D;154
4.3.2.6.2;Gene Signatures of HIV-VLPs Vaccine;156
4.3.2.6.3;Polymorphisms and Response to Measle Vaccine;157
4.3.2.6.4;Polymorphisms and Response to Rubella Vaccine;158
4.3.2.6.5;Polymorphisms and Response to Pertussis Vaccine;159
4.3.3;Conclusions;160
4.3.4;References;161
4.4;Immune Signatures Associated with the Cancer Bearing State;170
4.4.1;Background;170
4.4.2;Signatures of Immune Dysfunction in Cancer Patients;171
4.4.2.1;Increased Apoptosis of Anti-Tumor Effector Cells;171
4.4.2.2;Impaired Effector Cell Activation and Function;172
4.4.2.3;Polarizing Immune Balance in Favor of Tumor Progression;173
4.4.3;Signatures of Tumor Rejection in Cancer Patients;175
4.4.4;Applications of Cancer-Associated Immune Signatures in Therapeutics and Diagnostics;178
4.4.4.1;Therapeutics;178
4.4.4.2;Prognostic and Predictive Cancer Testing;179
4.4.5;Summary;180
4.4.6;References;180
5;Part IV:Tissue-Specific Patterns Associated with Chronic Inflammatory Processes;188
5.1;HTLV-1 Infected CD4+CD25+CCR4+ T-Cells Disregulate Balance of Inflammation and Tolerance in HTLV-1 Associated Neuroinflammatory Disease;189
5.1.1;Human T-Lymphotropic Virus Type 1 (HTLV-1)and Associated Disorders;189
5.1.2;Immunopathogenesis of HAM/TSP;190
5.1.3;HTLV-1 and Regulatory T-Cells;192
5.1.4;HTLV-1 Infected Foxp3 CD4+CD25+CCR4+ T-Cells Are Proinflammatory and Increased in HAM/TSP Patients;192
5.1.5;Do THAM Cells Include exFoxp3+ Cells?;195
5.1.6;References;196
5.2;D/2 Predictors of Favorable Outcome in Cancer;199
5.2.1;Predictors of Favorable Outcome in Colorectal Cancer;200
5.2.2;Predictors of Favorable Outcome in Other Cancers;203
5.2.3;Immunotherapy in Cancer;206
5.2.4;Summary;208
5.2.5;References;208
5.3;The Microenvironment of Ovarian Cancer: Lessons on Immune Mediated Tumor Rejection or Tolerance;211
5.3.1;Introduction;211
5.3.1.1;T Cells in Ovarian Cancer and Their Correlation with Outcome;212
5.3.1.2;Polyfunctional T Cells Are Present in the OvarianCancer Microenvironment;214
5.3.1.3;Chemokines Recruiting Antitumor T Cells to the Tumor Microenvironment;217
5.3.1.4;Regulatory T Cells, Presence and Outcome;218
5.3.1.5;The Tumor Endothelial Barrier: Another Layer of Immune Regulation;219
5.3.2;Conclusions;223
5.3.3;References;223
5.4;Transcriptional Profiling of Melanoma as a Potential Predictive Biomarker for Response to Immunotherapy;229
5.4.1;Analysis of T Cell Responses in the Peripheral Blood with Melanoma Vaccines;230
5.4.2;Interrogation of the Melanoma Tumor Microenvironment;230
5.4.3;Chemokines and an Argument for Control at the Level of T Cell Trafficking into Tumor Site;232
5.4.4;Innate Immune Signals that May Drive “Sterile” Adaptive Immunity to Tumors;232
5.4.5;Immune Suppressive Mechanisms in the Tumor Microenvironment;233
5.4.6;Analysis of the Tumor Microenvironment with Other Immunotherapy Approaches: IL-2 and Anti-CTLA-4 mAb;234
5.4.7;Conclusions and Future Directions;235
5.4.8;References;236
5.5;Functional Pathway Analysis for Understanding Immunologic Signature of Rejection: Current Approaches and Outstanding Challenges;239
5.5.1;Introduction;239
5.5.2;Insights from Application of Microarrays in Solid Organ Transplant;241
5.5.3;Need for Functional Pathway Analysis;244
5.5.4;Current Functional Pathway Analysis Approaches and Existing Tools;245
5.5.5;Over-Representation Analysis (ORA) Approaches;245
5.5.6;Functional Class Scoring (FCS) Approaches;247
5.5.7;Pathway Topology (PT)-Based Approaches;249
5.5.8;Outstanding Challenges;251
5.5.9;References;252
6;Part V:Signatures Associatedwith Acute Rejection;257
6.1;Chronic Graft Versus Host Disease: Inflammation at the Crossroads of Allo and Auto Immunity;258
6.1.1;Acute GVHD: Initiation of Inflammation, Recruitment of Effectors and T Lineage Determined Tissue Damage;260
6.1.2;CGVHD: Consequences of Chronic Inflammation in Tissues, Humoral Immunity and Fibrosis;262
6.1.3;Systemic Involvement of IFN in CGVHD;265
6.1.4;CGVHD: Chronic Fibrosis;266
6.1.5;CGVHD as an Autoimmune Disorder of Dysregulated Immunity;268
6.1.6;Conclusion;273
6.1.7;References;274
6.2;Immune-Mediated Tumor Rejection;280
6.2.1;The Current Understanding of Immune Surveillance and Its Molecular Basis;281
6.2.2;Strategies to Understand the Mechanism of Tumor Rejection;283
6.2.3;Immunological Signatures from the Tumor Microenvironment;286
6.2.4;Immune Aspects of Chemotherapy;290
6.2.5;Immune Aspects of Viral Oncolytic Therapy;293
6.2.6;Immune-Mediated Tumor Rejection as a Mechanism Shared by Other Pathologies: The Immunologic Constant of Rejection;295
6.2.7;Conclusions;296
6.2.8;References;297
6.3;Signatures Associated with Acute Rejection: Allograft Rejection;304
6.3.1;A Brief Historical Perspective;305
6.3.2;Introduction;306
6.3.3;Early Studies in Kidney and Liver Acute Allograft Rejection and the Detection of Recurrent Themes;307
6.3.4;Studies in Heart and Lung Acute Allograft Rejection, and Continuum from Acute to Chronic Rejection;324
6.3.5;Acute Allograft Rejection in Heterogeneous Condition and the Emerging Role of B Cells;326
6.3.6;Other Studies in Kidneys Acute Allograft Rejection, Role of IL-10, and Molecular Analogies Among Cellular and Humoral Rejection;327
6.3.7;Comparative Analyses and Role of STAT-1/IRF-1 and NF-kB;329
6.3.8;Conclusions;334
6.3.9;References;335
7;Index;345