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Th1 and Th2 cells, representing extremely polarized modalities of the specific effector immune response, play an important role in both protection against exogenous insults and the induction of several immunopathological reactions. This book provides an authoritative update on the developments in this fast-moving field from both basic and clinical perspectives. In 12 detailed chapters, leading immunologists highlight the physiological meaning of Th1 and Th2 cells, their functional properties and surface markers, the mechanisms responsible for their development, as well as their roles in protection against bacteria, protozoans, fungi, viruses and helminths. Also discussed are the roles of Th1 and Th2 cells in some immunopathological conditions, such as autoimmune and neurological disorders, allergy and HIV infection. By combining for the first time complete information on basic mechanisms together with the clinical implications of Th1/Th2-dominated immune responses, this book will be appreciated by a broad spectrum of readers, including immunobiologists and clinicians from many medical fields.
“About 25 years ago, Mosmann & Coffman introduced the TH1 / TH2 paradigm of T helper cell differentiation which helped explain many aspects of adaptive immunity from eliminating intracellular versus extracellular pathogens to induction of different types of tissue inflammation. However, TH1 / TH2 paradigm could not adequately explain development of certain inflammatory responses which provided impetus for the discovery of a new subset of T cells called TH17 cells. After the discovery of differentiation and transcription factors for TH17 cells, it was clear that TH17 cells represent an independent subset of T cells with specific functions in eliminating certain extracellular pathogens, presumably not adequately handled by TH1 or TH2 cells. The major role of TH17 cells has been described in inducing auto-immune tissue inflammation. The discovery of TH17 cells has expanded the TH1 / TH2 paradigm, and the integration of TH17 cells with TH1 and TH2 effector T cells is beginning to explain the underlying mechanisms of tissue inflammation in a number of infections and auto-immune disease settings.” - From Chapter One by Vijay K. Kuchroo, Harvard University, USA “The recently identified Interleukin 17 (IL-17) cytokine family contributes to immunity to infectious diseases and chronic inflammatory diseases. Further studies on the regulation and function of this important cytokine family may provide better understanding on the roles of the IL-17 family in immune-mediated diseases; such knowledge may lead to the development of immunotherapeutic strategies for treatment of several inflammatory diseases.” - From Chapter Two by Chen Dong, University of Texas and MD Anderson Cancer Center, USA
“About 25 years ago, Mosmann & Coffman introduced the TH1 / TH2 paradigm of T helper cell differentiation which helped explain many aspects of adaptive immunity from eliminating intracellular versus extracellular pathogens to induction of different types of tissue inflammation. However, TH1 / TH2 paradigm could not adequately explain development of certain inflammatory responses which provided impetus for the discovery of a new subset of T cells called TH17 cells. After the discovery of differentiation and transcription factors for TH17 cells, it was clear that TH17 cells represent an independent subset of T cells with specific functions in eliminating certain extracellular pathogens, presumably not adequately handled by TH1 or TH2 cells. The major role of TH17 cells has been described in inducing auto-immune tissue inflammation. The discovery of TH17 cells has expanded the TH1 / TH2 paradigm, and the integration of TH17 cells with TH1 and TH2 effector T cells is beginning to explain the underlying mechanisms of tissue inflammation in a number of infections and auto-immune disease settings.” - From Chapter One by Vijay K. Kuchroo, Harvard University, USA “The recently identified Interleukin 17 (IL-17) cytokine family contributes to immunity to infectious diseases and chronic inflammatory diseases. Further studies on the regulation and function of this important cytokine family may provide better understanding on the roles of the IL-17 family in immune-mediated diseases; such knowledge may lead to the development of immunotherapeutic strategies for treatment of several inflammatory diseases.” - From Chapter Two by Chen Dong, University of Texas and MD Anderson Cancer Center, USA
Methods in Toxicology, Volume 2: Mitochondrial Dysfunction provides a source of methods, techniques, and experimental approaches for studying the role of abnormal mitochondrial function in cell injury. The book discusses the methods for the preparation and basic functional assessment of mitochondria from liver, kidney, muscle, and brain; the methods for assessing mitochondrial dysfunction in vivo and in intact organs; and the structural aspects of mitochondrial dysfunction are addressed. The text also describes chemical detoxification and metabolism as well as specific metabolic reactions that are especially important targets or indicators of damage. The methods for measurement of alterations in fatty acid and phospholipid metabolism and for the analysis and manipulation of oxidative injury and antioxidant systems are also considered. The book further tackles additional methods on mitochondrial energetics and transport processes; approaches for assessing impaired function of mitochondria; and genetic and developmental aspects of mitochondrial disease and toxicology. The text also looks into mitochondrial DNA synthesis, covalent binding to mitochondrial DNA, DNA repair, and mitochondrial dysfunction in the context of developing individuals and cellular differentiation. Microbiologists, toxicologists, biochemists, and molecular pharmacologists will find the book invaluable.
The two major subsets of CD4+ helper T cells, designated Th1 and Th2, have quite different patterns of cytokine production and, as a consequence, have very different roles in immune responses. The articles in this volume review both basic and clinical studies of T cell heterogeneity, including: the mechanisms by which Th1 and Th2 cells develop and maintain their differences in cytokine production; the different roles of Th1 and Th2 cells in allergy, autoimmunity and infectious diseases; the prospects and strategies for therapeutic manipulation of Th1 and Th2 cells; and the control of Th1 and Th2 responses by regulatory T cell subsets. The volume should give the reader a view of the development and function of Th1 and Th2 cells and the attempts to treat immunological diseases with therapies directed towards altering the Th1/Th2 balance.
This book explains how stress – either psychological or physical – can activate and/or paralyse human innate or adaptive immunity. Adequate immunity is crucial for maintaining health, both on Earth and in space. During space flight, human physiology is specifically challenged by complex environmental stressors, which are most pronounced during lunar or interplanetary missions. Adopting an interdisciplinary approach, the book identifies the impact of these stressors – the space exposome – on immunity as a result of (dys-)functions of specific cells, organs and organ networks. These conditions (e.g. gravitation changes, radiation, isolation/confinement) affect immunity, but at the same time provide insights that may help to prevent, diagnose and address immune-related health alterations. Written by experts from academia, space agencies and industry, the book is a valuable resource for professionals, researchers and students in the field of medicine, biology and technology. The chapters “The Impact of Everyday Stressors on the Immune System and Health”, “Stress and Radiation Responsiveness” and “Assessment of Radiosensitivity and Biomonitoring of Exposure to Space adiation” are available open access under a Creative Commons Attribution 4.0 International License via link.springer.com.
The Janeway's Immunobiology CD-ROM, Immunobiology Interactive, is included with each book, and can be purchased separately. It contains animations and videos with voiceover narration, as well as the figures from the text for presentation purposes.
This new edition is a unique combined resource for physicians and scientists addressing the needs of both groups. In addition to stimulating exchange and collaboration and shortening the path between discovery and application of new knowledge, the book helps clinicians understand new therapeutic concepts from their origins. The volume serves as a comprehensive guide to the current diagnostic modalities, including enhanced imaging techniques such as MRI and CT enterography, virtual colonoscopy, ultrasound, and endomicroscopy, as well as conventional and complex immunomodulatory principles. The latest edition also includes revised chapters from the previous edition, as well as new chapters reflecting current developments in the field. Written by experts in their field, Crohn’s Disease and Ulcerative Colitis: From Epidemiology and Immunobiology to a Rational Diagnostic and Therapeutic Approach, Second Edition is of great value to gastroenterologists, surgeons, internists, pediatricians and gynecologists trainees, as well as all those involved in Crohn’s disease, ulcerative colitis, and related autoimmune disorders.
Macrophages have unique and diverse functions necessary for survival. And, in humans (and other species), they are the most abundant leukocytes in tissues. The Innate functions of macrophages that are best known are their unusual ability to either “Kill” or “Repair”. Since killing is a destructive process and repair is a constructive process, it was stupefying how one cell could exhibit these 2 polar – opposite functions. However, in the late 1980’s, it was shown that macrophages have a unique ability to enzymatically metabolize Arginine to Nitric Oxide (NO, a gaseous non – specific killer molecule) or to Ornithine (a precursor of polyamines and collagen for repair). The dual Arginine metabolic capacity of macrophages provided a functional explanation for their ability to kill or repair. Macrophages predominantly producing NO are called M1 and those producing Ornithine are called M2. M1 and M2 – dominant responses occur in lower vertebrates, and in T cell deficient vertebrates being directly driven by Damage and Pathogen Associated Molecular Patterns (DAMP and PAMP). Thus, M1 and M2 are Innate responses that protect the host without Adaptive Immunity. In turn, M1/M2 is supplanting previous models in which T cells were necessary to “activate” or “alternatively activate” macrophages (the Th1/Th2 paradigm). M1 and M2 macrophages were named such because of the additional key findings that these macrophages stimulate Th1 and Th2 – like responses, respectively. So, in addition to their unique ability to kill or repair, macrophages also govern Adaptive Immunity. All of the foregoing would be less important if M1 or M2 – dominant responses were not observed in disease. But, they are. The best example to date is the predominance of M2 macrophages in human tumors where they act like wound repair macrophages and actively promote growth. More generally, humans have become M2 – dominant because sanitation, antibiotics and vaccines have lessened M1 responses. And, M2 dominance seems the cause of ever - increasing allergies in developed countries. Obesity represents a new and different circumstance. Surfeit energy (e.g., lipoproteins) causes monocytes to become M1 dominant in the vessel walls causing plaques. Because M1 or M2 dominant responses are clearly causative in many modern diseases, there is great potential in developing the means to selectively stimulate (or inhibit) either M1 or M2 responses to kill or repair, or to stimulate Th1 or Th2 responses, depending on the circumstance. The contributions here are meant to describe diseases of M1 or M2 dominance, and promising new methodologies to modulate the fungible metabolic machinery of macrophages for better health.