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.

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 volume details our current understanding of the architecture and signaling capabilities of the B cell antigen receptor (BCR) in health and disease. The first chapters review new insights into the assembly of BCR components and their organization on the cell surface. Subsequent contributions focus on the molecular interactions that connect the BCR with major intracellular signaling pathways such as Ca2+ mobilization, membrane phospholipid metabolism, nuclear translocation of NF-kB or the activation of Bruton’s Tyrosine Kinase and MAP kinases. These elements orchestrate cytoplasmic and nuclear responses as well as cytoskeleton dynamics for antigen internalization. Furthermore, a key mechanism of how B cells remember their cognate antigen is discussed in detail. Altogether, the discoveries presented provide a better understanding of B cell biology and help to explain some B cell-mediated pathogenicities, like autoimmune phenomena or the formation of B cell tumors, while also paving the way for eventually combating these diseases.

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.