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The prevalence of asthma has markedly increased in recent decades. Asthma affects approximately ten percent of the population of the United States, and is the leading cause of childhood hospitalization. This epidemic has been attributed to air pollution, childhood immunizations and a more sanitary living environment. Allergic asthma is clinically characterized by airway hyperreactivity (AHR), increased mucus production and airway remodeling. On the cellular level, pulmonary eosinophilic infiltration and augmented levels of serum IgE arise as a consequence of a CD4+ Th2 cell response in the airway following exposure to allergen. It has been proposed that the chronic inflammation and associated airway events evident in this disease stem from a failure to regulate the underlying immune response. How these events are regulated in the healthy lung is yet unclear. In studies to investigate the mechanisms underlying such regulation we found that firstly, co-transfer of expanded natural CD4+ CD25+ Foxp3+ regulatory T cells (nTregs) mediated regulation of CD4+ Th17 effector cells as exemplified by diminished levels of IL-17 and decreased neutrophilic infiltration in the airways. In contrast, co-transfer of nTregs did not attenuate the lung inflammation elicited by CD4+ Th2 or Th1 polarized cells. Interestingly, using the C129. IL4GFP mice we found that nTregs have the capacity to inhibit IL-4 production and Th2 differentiation in vitro. Secondly, mice with genetically disrupted receptors (IP-/- ) for the lipid-mediator prostacyclin (PGI2), demonstrated increased airway inflammation, eosinophilic infiltration and airway hyperreactivity following immunization and repeated aerosol challenge with ovalbumin. Moreover these mice displayed reduced serum immunoglobulin levels. In summary, nTregs serve a specific function in controlling Th17 cell effector functions, but not Th1 or Th2 inflammation. Additionally, PGI2-IP signaling is an important pathway for inhibiting allergic pulmonary inflammation by controlling CD4+ Th2 cell effector functions.
Eosinophils represent approximately 1% of peripheral blood leukocytes and play a central proinflammatory and immunoregulatory role in various immune disorders. This volume provides the reader with a comprehensive survey of the major aspects of human eosinophilic biology and immunology as well as the most clinically relevant aspects of eosinophil-related disorders. Expert contributions cover the ultrastructural and phenotypic characteristics of human eosinophils, and their fundamental biochemical features including receptors for IgE and chemokines. The production of cytokines and their role in the activation of eosinophils are reviewed. Furthermore, the classic eosinophil-related disorders such as hypereosinophilia, drug reactions, allergic disorders and some cardiovascular diseases are described. Each of the chapters is written by an investigator actively engaged in research on the topic under consideration. The well-edited and stimulating material compiled in this volume will be of interest to all those working in allergology, immunology, biochemistry and pulmonary medicine.
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.
"Allergic diseases are the result of an aberrant immune response by T helper type 2 cells to allergens. Allergic sensitization is considered to be a multifactorial process that involves among others, environmental factors, genetics and characteristics of allergens. In normal conditions, exposure to non-infectious protein antigens induces a state of tolerance, which is essential to maintain homeostasis under constant exposure to environmental antigens. A failure in the mechanisms of tolerance, leads to activation of pro-inflammatory pathways and the development of allergen specific T cell responses. The development of animal models of various allergies has been beneficial in allowing extensive investigations into mechanisms involved in the allergic pathways. These animal models can be used to predict potential risk factors as well as to test novel treatments and immunotherapy. The risk of anaphylaxis in humans is a limiting factor for the development of allergen-based immunotherapy. In this context, animal models can play an essential role in providing a platform for refining therapeutic treatments and ensuring safety, prior to application in humans. In this thesis we use animal models to address essential questions such as what makes an individual respond to allergens. We have studied this question from different perspectives and have identified a role for the capacity to cope with allergen induced oxidative stress; the role of epithelial contact with HDM allergens in the development of an IgE response; the immunological interplay between allergic immune responses directed against unrelated allergens in different compartments of the body and; the immunological interplay between cross-reactive allergens."--Samenvatting auteur.
Asthma, allergy and chronic obstructive lung disease are common throughout the world and are increasing in incidence, particularly in the developing world. This volume provides a state-of-the-art account of the identification of new targets and the development of new therapies for these conditions. Some 40 chapters by clinical academics and senior members of the pharmaceutical industry detail the latest breakthroughs in research and development. In asthma, a promising approach is the use of therapy directed against specific Th2 responses through biological antagonists of IL-5, IL-4 and IL-13. There have also been major advances in our understanding of innate immune responses to pathogen-associated molecular patterns, and in the area of Toll-like receptors. Up to date and comprehensive, this book will be of particular relevance to those working in the pharmaceutical industry (in preclinical research and clinical development), to academic researchers in the field of respiratory medicine, and to respiratory health care specialists.
From 1962 to 1971, the U.S. military sprayed herbicides over Vietnam to strip the thick jungle canopy that could conceal opposition forces, to destroy crops that those forces might depend on, and to clear tall grasses and bushes from the perimeters of US base camps and outlying fire-support bases. Mixtures of 2,4-dichlorophenoxyacetic acid (2,4-D), 2,4,5-trichlorophenoxyacetic acid (2,4,5-T), picloram, and cacodylic acid made up the bulk of the herbicides sprayed. The main chemical mixture sprayed was Agent Orange, a 50:50 mixture of 2,4-D and 2,4,5-T. At the time of the spraying, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), the most toxic form of dioxin, was an unintended contaminant generated during the production of 2,4,5-T and so was present in Agent Orange and some other formulations sprayed in Vietnam. Because of complaints from returning Vietnam veterans about their own health and that of their children combined with emerging toxicologic evidence of adverse effects of phenoxy herbicides and TCDD, the National Academies of Sciences, Engineering, and Medicine was asked to perform a comprehensive evaluation of scientific and medical information regarding the health effects of exposure to Agent Orange, other herbicides used in Vietnam, and the various components of those herbicides, including TCDD. Updated evaluations were conducted every two years to review newly available literature and draw conclusions from the overall evidence. Veterans and Agent Orange: Update 11 (2018) examines peer-reviewed scientific reports concerning associations between various health outcomes and exposure to TCDD and other chemicals in the herbicides used in Vietnam that were published between September 30, 2014, and December 31, 2017, and integrates this information with the previously established evidence database.
Animal models are indispensable for studies requiring an intact immune system, especially for studying the pathogenic mechanisms in atopic diseases, regulation of IgE production, and related biologic effects. Mice are particularly suitable and have been used extensively for such studies because their immune system is well characterized. Further, large numbers of mutants or inbred strains of mice are available that express deficiencies of individual immunologic processes, inflammatory cells, or mediator systems. By comparing reactions in such mice with appropriate control animals, the unique roles of individual cells or mediators may be characterized more precisely in the pathogenesis of atopic respiratory diseases including asthma. However, given that asthma in humans is characterized by the presence of airway hyperresponsiveness to specific and nonspecific stimuli, it is important that animal models of this disease exhibit similar physiologic abnormalities. In the past, the size of the mouse has limited its versatility in this regard. However, recent studies indicate the feasibility of measuring pulmonary responses in living mice, thus facilitating the physiologic evaluation of putative mouse models of human asthma that have been well charcterized at the immunologic and patholigic level. Future work will provide details of the morphometry of the methacholine-induced bronchoconstriction and will further seek to determine the relationship between cigarette smoke exposure and the development of NS-AHR in the transgenic mouse model.