Acute Phase Proteins in the Acute Phase Response

Inhaltsverzeichnis

• 1 Interleukin-1 in the Acute Phase Response.
• The Acute Phase Response.
• Structure of IL-1.
• Synthesis and Regulation of IL-1.
• IL-1 Receptor.
• Pleotropic Actions of IL-1.
• IL-1 and Acute Phase Reactions.
• Fever.
• Leukocytosis.
• Acute Phase Proteins.
• IL-1 and Other Cytokines.
• Synergy of Action.
• Induction of Other Cytokines by IL-1.
• IL-1 and Corticosteroid.
• In Vivo Action of IL-1.
• Summary.
• 2 Regulation of Human SAA Gene Expression by Cytokines.
• In Vitro Expression of Human SAA.
• Cis-acting Sequences Responsible for PMA Induction of SAA.
• Cytokine Control of SAA Expression.
• 3 Transcriptional Regulation of Acute Phase Response Genes with Emphasis on the Human C-reactive Protein Gene.
• The Physiological Role of the Acute Phase Response.
• Systems for the Study of the Acute Phase Response.
• Monokines Responsible for the Modulation of Liver-specific Gene Expression.
• Transcriptional Regulation — the Mechanism.
• Liver-specific Promoters and Enhancers.
• Promoters Induced During the Acute Phase.
• Conclusions and Perspectives.
• 4 Organization, Structure and Expression of Pentraxin Genes.
• The Structure of Pentraxin Proteins.
• The Structure of Pentraxin Genes.
• Heat Shock Elements.
• The Purine-Pyrimidine Repeat Region and Oligo-A Stretch in the CRP Intron.
• The 3? Untranslated Region.
• Elements Responding to Cytokines.
• Genetics.
• 5 ApoSSA: Structure, Tissue Expression and Possible Functions.
• Background.
• SAA is an Apolipoprotein.
• Where are SAAs Made and Where do They go?.
• Patterns of Cell and Tissue Expression of SAA mRNAs in Mice.
• Rats Have SAA-related Genes.
• 6 Regulation of Biosynthesis and Secretion of Human C-reactive Protein and Serum Amyloid A.
• Regulation of Biosynthesis.
• Role of Cytokines.
• Role of Cofactors: Signal Transduction.
• Heterogeneity in the Acute Phase Response.
• Regulation of CRP Secretion.
• Dynamics of CRP Secretion by Rabbit.
• Hepatocytes.
• Subcellular Localization of the Intracellular Pool of CRP.
• CRP is Specifically Retained Within the Endoplasmic Reticulum.
• Conclusions.
• 7 Molecular Regulation of the Acute Phase Complement Proteins.
• Factor B.
• The Second Component, C2.
• Constitutive Expression of Factor B and C2.
• Regulated Gene Expression.
• Interleukin-1 and Interferon-?.
• Tumor Necrosis Factor and Interleukin-6.
• 8 Biosynthesis of Acute Phase Proteins by the Liver Cells.
• Role of Hepatocytes in the In Vivo Biosynthesis of APR.
• Expression of APR in the Normal Unstimulated Liver.
• Expression of APR During the AIR.
• Role of Sinusoidal Cells in the In Vivo Biosynthesis of APR.
• 9 The Plasma Serine Protease Inhibitors (Serpins): Structural Modifications in Inflammation.
• The Serpins.
• Structure of the Serpins.
• Synthesis of Serpins in Inflammation.
• Antitrypsin.
• Antitrypsin Deficiency.
• The Reactive Centre.
• Mechanism of Protease Inhibition.
• Specificity of Inhibition.
• Reactive Centre Oxidation of Antitrypsin.
• The SR Conformational Change.
• Physiological Significance of the SR Change.
• Pathological Significance of the SR Change.
• Evolutionary Loss of the SR Change.
• Other Structural Modifications in Inflammation.
• N-terminal Cleavage: Angiotensinogen.
• Modification of Carbohydrate.
• 10 The Three Dimensional Structure of SAP.
• 11 Structure, Metabolism and Function of Acute Phase High Density Lipoprotein.
• Apo-SAA in Plasma.
• Structure of Apo-SAA.
• Structure of Acute Phase HDL.
• Metabolic Function of Normal HDL.
• Synthesis of Apo-SAA.
• Plasma Clearance of Apo-SAA.
• Cellular Association and Degradation of Apo-SAA.
• Functions of Apo-SAA.
• Concluding Remarks.
• 12 Clinical Measurement of Acute Phase Proteins to Detect and Monitor Infectious Diseases.
• Microbial Growth and AP Protein Response.
• General Pattern of AP Protein Response in Infection.
• Monitoring Disease Activity Using AP Protein Response.
• AP Protein Response in Viral Infection.
• Immunomodulation and AP Protein Response.
• 13 C-reactive Protein: Clinical Aspects.
• The Acute Phase Proteins.
• The Erythrocyte Sedimentation Rate as an Indirect Indicator for the Acute Phase Reaction.
• C-reactive Protein as a Direct Indicator of the Acute Phase Reaction.
• Assays for CRP.
• CRP Levels in Different Diseases.
• Functions of CRP.
• Conclusion.
• 14 Pathogenesis of AA Amyloidosis.
• Definition and Classification of Amyloidosis.
• Serum and Tissue Amyloid A Proteins.
• Structure of SAA and AA.
• Induction and Production of the Acute Phase.
• Protein SAA.
• Apo SAA and “Apo AA”.
• Displacement of SAA from HDL-SAA Complexes by Apo AI and Apo AII.
• Formation and Deposition of AA Amyloid.
• Incomplete Degradation of SAA.
• Amyloid Enhancing Factor and Glycosaminoglycans.
• Protein AP: The Amyloid “P Component”.
• Summary of Some Current Hypotheses Regarding AA Amyloid Formation.
• 15 Serum Amyloid P Component: A Specific Molecular Targeting Vehicle in Amyloidosis.
• Serum Amyloid P Component.
• Ligand Binding by SAP/AP.
• Binding of SAP to Chromatin.
• SAP and Amyloidosis.
• Tissue Amyloid P Component.
• SAP as a Targeting Vehicle in Amyloidosis.
• Scintigraphic Imaging of Amyloid Deposits In Vivo.
• Radiolabelled-SAP Studies in Experimental Murine Amyloidosis.
• Mouse Imaging Studies Using 123I-Human SAP.
• Mouse Imaging Studies Using 123I-Mouse SAP.
• Localization of 125I-Pentraxins in AEF-Induced Amyloid.
• 125I-SAP Localization as a Method of Quantitating Murine Amyloid Deposits.
• Radiolabeled SAP Studies in Man.
• Preparation of 123I-Human SAP for Clinical Studies.
• Imaging of Human Amyloid Deposits.
• Human SAP Turnover Studies.