[PDF] Signal Transduction Pathways In Autoimmunity eBook
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The chapters included in this volume represent but a few examples of the close link between aberrant signaling pathways and autoimmune diseases. They cover a variety of cells (T, B and myeloid/monocytic cells), receptors (for antigen, Fc and cytokines) and intracellular signaling molecules (kinases, phosphatases, adapters and transcription factors) in the immune system. This book brings together clinical and experimental aspects of autoimmune disease and the fundamental science of intracellular signaling pathways. Therefore, it should be of interest to clinical investigators of autoimmune diseases as wll as to basic immunologists and cell biologists interested in the molecular basis of signal transduction in the immune system.
Protein phosphorylation via protein kinases is an inevitable process that alters physiological and pathological functions of the cells. Thus, protein kinases play key roles in the regulation of cell life or death decisions. Protein kinases are frequently a driving factor in a variety of human diseases including aging and cellular senescence, immune system and endothelial dysfunctions, cancers, insulin resistance, cholestasis and neurodegenerative diseases, as well as bacterial resistance in persistent infections. Recent developments in quantitative proteomics provide important opinions on kinase inhibitor selectivity and their modes of action in the biological context. Protein Kinase-mediated Decisions Between Life and Death aims to have the reader catch insights about up-to-date opinions on “Protein Kinases” related pathways that threaten human health and life. As “Protein Kinases” are related to many health problems, clinicians, basic science researchers and students need this information. Chapter “Signal Transduction in Immune Cells and Protein Kinases” is available open access under a Creative Commons Attribution 4.0 International License via link.springer.com.
Autoimmune disorders are known to affect a substantial number of people worldwide, demonstrating a gender bias and are the second largest cause of chronic illness. Recently, the attention has been focused on lifestyle changes as a major factor in the rise of autoimmune disease frequency. The two sections of this book are focused on the new opportunities for moving research forward, leading to a new approach to prevention and treatment of autoimmune diseases. A better understanding of the mechanisms of gene expression and triggering signaling pathways, which is involved in autoimmune pathogenesis simultaneously with current data for the interaction of microbiota with human immune system, will help to better understand the immune imbalance implicated in autoimmunity.
Author : Keith B. Elkon Publisher : Karger Medical and Scientific Publishers Page : 228 pages File Size : 20,72 MB Release : 2006 Category : Medical ISBN :
Over the last 15 years, apoptosis has become a dominant focus of medical research in the field of immunology. This publication discusses the three major areas of apoptosis research: extrinsic death receptor pathways, intrinsic cell death pathways and the mechanisms responsible for apoptotic cell clearance. Each section delineates the proteins and signal transduction pathways and describes genetic alterations that lead to autoimmune diseases. Although most cell death abnormalities have been associated with systemic autoimmune disorders such as lupus erythematosus and lymphoproliferative syndromes, it is evident that regulation of cell death is also pertinent to disease expression in many organ-specific diseases such as rheumatoid arthritis and glomerulonephritis. This volume highlights the recent advances in the basic mechanisms of apoptosis and the application of that knowledge to understanding the impact of defective apoptosis or defective clearance of apoptotic cells on the immune function and the expression of disease. It is of special interest to cell biologists, immunologists and clinicians.
This book comprehensively sets out the common aetiopathogenetic mechanisms shared by many, apparently diverse, diseases of the immune system. Unlike most other texts it does not emphasise the differences between autoimmune diseases, but establishes their many common links including hormonal effects, dietary and immunogenetic influences, complement deficiencies and environmental factors. Special attention is given to the effects of ageing and the relationship with malignancies. The scope of the book is very broad so as to cover the integration of the many diverse components which interact to cause autoimmunity, and it contains many 1988 and 1989 references and over 100 figures and tables, offering an attractive, up-to-date guide to modern concepts. It will greatly assist immunologists wishing to enter the field of autoimmunity, and will serve as an invaluable reference work for those already working in it.
Author : David A. Frank Publisher : Springer Science & Business Media Page : 358 pages File Size : 27,82 MB Release : 2002-12-31 Category : Medical ISBN : 1402073402
One of the most exciting areas of cancer research now is the development of agents which can target signal transduction pathways that are activated inappropriately in malignant cells. The understanding of the molecular abnormalities which distinguish malignant cells from their normal counterparts has grown tremendously. This volume summarizes the current research on the role that signal transduction pathways play in the pathogenesis of cancer and how this knowledge may be used to develop the next generation of more effective and less toxic anticancer agents. Series Editor comments: "The biologic behavior of both normal and cancer cells is determined by critical signal transduction pathways. This text provides a comprehensive review of the field. Leading investigators discuss key molecules that may prove to be important diagnostic and/or therapeutic targets."
The mechanisms of idiosyncratic drug reactions (IDRs) are unknown; however, most appear to be immune-mediated. Their idiosyncratic nature and the paucity of animal models make mechanistic studies very difficult. One of the few animal models is penicillamine-induced autoimmunity in Brown Norway rats. The major focus of this thesis was the use of this model to study the interaction between penicillamine and macrophages, the involvement of Th17 cells, and extension of this model to idiosyncratic drug-induced liver injury. Th17 cells are prominent in autoimmune syndromes and Th17-associated cytokines such as IL-17 were elevated in the penicillamine-treated animals that developed autoimmunity. We have hypothesized that some drug-induced liver injury has an autoimmune component. A pilot study quantified serum concentrations of 26 cytokines/chemokines in patients with various forms of acute liver failure (ALF): idiosyncratic drug-induced ALF, acetaminophen-induced ALF, and viral hepatitis. IL-17 was elevated in 60% of patients with idiosyncratic drug-induced ALF, which supports an autoimmune component in these patients; however, it was also elevated in many cases of acetaminophen-induced ALF, presumably released by the innate immune system. These studies provide important insights into the mechanism of penicillamine-, hydralazine-, and isoniazid-induced autoimmunity and also provide clues to other IDRs that may have an autoimmune component. One of the costimulatory signals leading to T cell activation appears to be reversible Schiff-base formation between an amine on T cells and an aldehyde on macrophages. We hypothesized that penicillamine binds to these aldehydes leading to macrophage activation and autoimmunity. By using biotinylated aldehyde-reactive agents such as ARP, we demonstrated the existence of aldehydes on the surface of macrophages. We synthesized biotinylated-penicillamine and it also binds to macrophages. Several proteins to which ARP binds were identified providing clues to the signal transduction pathways leading to macrophage activation. Biological consequences of this binding were investigated with a microarray study. ARP binding was also observed in the macrophage cell line, RAW264.7, and incubation with penicillamine stimulated the production of TNF-alpha, IL-6, and IL-23. Hydralazine and isoniazid, which are known to cause a lupus-like syndrome in humans and irreversibly bind to aldehyde groups, were also found to activate RAW264.7 cells.
This book uniquely relates the broad impact of signal transduction research on the understanding and treatment of human disease. There have been significant advances in the area of signaling in disease processes, yet no resource presently connects these advances with understanding of disease processes and applications for novel therapeutics. Given the emphasis on translational research and biological relevance in biotechnology, and, conversely, the importance of molecular approaches for clinical research, it is evident that a single resource bridging signaling research and human disease will be invaluable.
T cells play a vital role mediating adaptive immunity, a specific acquired resistance to an infectious agent produced by the introduction of an antigen. There are a variety of T cell types with different functions. They are called T cells, because they are derived from the thymus gland. This volume discusses how T cells are regulated through the operation of signaling mechanisms. Topics covered include positive and negative selection, early events in T cell receptor engagement, and various T cell subsets.