The Immunological Basis Of Asthma

This text assesses the role of dendritic cells, T and B lymphocytes, epithelial and mast cells, eosinophils, neutrophils, macrophages, and their products in the initiation and progression of airway inflammation, regulation, and repair. It unveils advances in immunology and cell biology to generate new therapeutic regimens for inflammatory and aller

This book explores the cellular and molecular mechanisms involved in asthma and allergic diseases, from basic immunology to the treatment of patients. Arising from a special symposium held to celebrate Professor A. Barry Kay's 20th anniversary as Head of the Department of Allergy and Clinical Immunology at the National Heart and Lung Institute, London, the publication presents 18 review articles by an impressive cross section of experts in the field. Topics considered include Th1 and Th2 cells, the regultion of Th2 cytokine transcription, the role of T cells in the immunopathogenesis of asthma, and MHC-restricted IgE-independent T-cell-induced late-phase responses in human subjects. Further chapters focus on eosinophil adhesion and activation, the role of C-C chemokines in the recruitment of eosinophils, and the interactions between eosinophils and fibroblasts. T-cell recruitment and T-cell interactions in cutaneous basophil hypersensitivity and fibrotic lung disease are discussed, as is the molecular pathology of allergic disease. Finally, treatment approaches are considered in chapters on the molecular basis of corticosteroid actions in asthma, immunosuppression in asthma, and immunotherapy of allergic diseases.

This first volume of the comprehensive, two-volume work on oxidative stress in lung disease introduces the molecular mechanisms, and the role of oxidants in the progression of different lung diseases. The lungs of humans and animals are under constant threat from oxidants from either endogenous (e.g. in situ metabolic reactions) or exogenous sources (e.g. air pollutants). Further, oxidative stress causes the oxidation of proteins, DNA and lipids, which in turn generates secondary metabolic products. The book consists of sections, each focusing on different aspects of oxidant-mediated lung diseases. As such it is a unique reference resource for postgraduate students, biomedical researchers and also for the clinicians who are interested in studying and understanding oxidant-mediated lung diseases. The second volume will incorporate other aspects of oxidant-mediated lung diseases, including prevention and therapeutics.

Severe asthma is a form of asthma that responds poorly to currently available medication, and its patients represent those with greatest unmet needs. In the last 10 years, substantial progress has been made in terms of understanding some of the mechanisms that drive severe asthma; there have also been concomitant advances in the recognition of specific molecular phenotypes. This ERS Monograph covers all aspects of severe asthma – epidemiology, diagnosis, mechanisms, treatment and management – but has a particular focus on recent understanding of mechanistic heterogeneity based on an analytic approach using various ‘omics platforms applied to clinically well-defined asthma cohorts. How these advances have led to improved management targets is also emphasised. This book brings together the clinical and scientific expertise of those from around the world who are collaborating to solve the problem of severe asthma.

Asthma is a prevalent disease in all age groups that results from different pathogenic mechanisms, cells, and mediators engaged in innumerous clinical phenotypes and endotypes. This book exhaustively and didactically explores the biological expression of numerous cells and mediators involved in bronchial inflammation. The information provided aims at identifying the diversity and complexity of the interrelationships between the different players, drawing attention to critical mechanisms in asthma. It also highlights the requirement of new tools to identify strong biomarkers absolutely critical for managing asthma.