The relationship between infection and immunity and autophagy, a pathway of cellular homeostasis and stress response, has been a rapidly growing field of study over the last decade. While some cellular processes are pro- or anti-infection, autophagy has been proven to be both: a part of the innate immune response against some microbes, and a cellular pathway subverted by some pathogens to promote their own replication. Autophagy, Infection, and the Immune Response provides a unified overview of the roles of cellular autophagy during microbial infection. Introductory chapters ground the reader by delineating the autophagic pathway from a cellular perspective, and by listing assays available for measuring autophagy. Subsequent chapters address virus interactions with autophagy machinery, the various roles of autophagy parasitic infection, and interactions of bacteria with the autophagic pathway. Concluding chapters explore the relationships of autophagy to systemic immune responses, including antigen presentation, ER stress, and production of IFN-gamma. Designed as a resource for those interested in initiating studies on the relationship between autophagy and infection or immunity, Autophagy, Infection, and the Immune Response combines practical state-of the art technique descriptions with an overview of the wide variety of known interactions between pathogens and the autophagic pathway.

Autophagy is a fundamental biological process that enables cells to autodigest their own cytosol during starvation and other forms of stress. It has a growing spectrum of acknowledged roles in immunity, aging, development, neurodegeneration, and cancer biology. An immunological role of autophagy was first recognized with the discovery of autophagy’s ability to sanitize the cellular interior by killing intracellular microbes. Since then, the repertoire of autophagy’s roles in immunity has been vastly expanded to include a diverse but interconnected portfolio of regulatory and effector functions. Autophagy is an effector of Th1/Th2 polarization; it fuels MHC II presentation of cytosolic (self and microbial) antigens; it shapes central tolerance; it affects B and T cell homeostasis; it acts both as an effector and a regulator of Toll-like receptor and other innate immunity receptor signaling; and it may help ward off chronic inflammatory disease in humans. With such a multitude of innate and adaptive immunity functions, the study of autophagy in immunity is one of the most rapidly growing fields of contemporary immunological research. This book introduces the reader to the fundamentals of autophagy, guides a novice and the well-informed reader alike through different immunological aspects of autophagy as well as the countermeasures used by highly adapted pathogens to fight autophagy, and provides the expert with the latest, up-to-date information on the specifics of the leading edge of autophagy research in infection and immunity.

Understanding the importance and necessity of the role of autophagy in health and disease is vital for the studies of cancer, aging, neurodegeneration, immunology, and infectious diseases. Comprehensive and up-to-date, this book offers a valuable guide to these cellular processes whilst encouraging researchers to explore their potentially important connections. Volume 3 explores the role of autophagy in specific diseases and developments, including: Crohn's Disease, Gaucher Disease, Huntington's Disease, HCV infection, osteoarthritis, and liver injury. A full section is devoted to in-depth exploration of autophagy in tumor development and cancer. Finally, the work explores the relationship between autophagy and apoptosis, with attention to the ways in which autophagy regulates apoptosis, and the ways in which autophagy has been explored in Lepidoptera, elucidating the use of larval midgut as a model for such exploration. From these well-developed foundations, researchers, translational scientists, and practitioners may work to better implement more effective therapies against some of the most devastating human diseases. Volumes in the Series

Autophagy in Immune Response: Impact on Cancer Immunotherapy focuses on the status and future directions of autophagy with respect to different aspects of its interaction with the immune system and immunotherapy. The book takes scientific research in autophagy a step further by presenting reputable information on the topic and offering integrated content with advancements in autophagy, from cell biology and biochemical research, to clinical treatments. This book is a valuable source for cancer researchers, oncologists, graduate students and several members of biomedical field who are interested in learning more on the relationship between autophagy and immunotherapies. - Presents updated knowledge on autophagy at the basic level and its potential use in cancer treatment - Offers the first book to cover autophagy at the interface of cell biology, immunology and tumor biology - Provides a wealth of information on the topic in a coherent and comprehensive collection of contributions by world renowned scientists and investigators

Over the last years it has become evident that many neurological diseases of the central nervous system (CNS) are induced by a specific adaptive immune response directed against molecules expressed on CNS-resident cells. Well-recognized examples are anti-N-Methyl-D-Aspartate Receptor (NMDAR) encephalitis which is characterized by the presence of antibodies against neuron-expressed NMDAR, or neuromyelitis optica (NMO), induced by antibodies to astrocyte-expressed aquaporin-4. Many more examples exist, and antibodies, and T or/and B cells have increasingly been associated with CNS disease. Often the symptoms of these diseases have not been typically reported to have an immune aetiology. Beside classical neurological symptoms like ataxia, vision disturbance, and motor or sensory symptoms, these can include cognitive disturbances, behavioral abnormalities, or/and epileptic seizures. Although much has been learned regarding the pathophysiology of prototypic examples of these disorders, there are still major gaps in our understanding of their biology. This may be due to the fact that they are rare diseases, and their therapies are still very limited. This research topic includes contributions addressing the analysis of the adaptive immune response driving disease including target antigens, molecular epitope mapping, and factors involved in the disease pathogenesis such as complement activation cascades, genetic and genomic regulation, as well as environmental triggers. Diagnostic criteria and methods, and treatment are also discussed. The overall aim of the volume is to review progress in our pathophysiological understanding of immune-mediated CNS disorders in order to advance diagnostic and therapeutic approaches, and ultimately improve outcomes for patients.

The use of model antigens such as haptens and ovalbumin has provided enormous insights into how immune responses develop, particularly to vaccine antigens. Furthermore, these studies are overwhelmingly performed in animals housed in clean facilities and are not known to have experienced overt clinical signs caused by infectious agents. Therefore, this is unlikely to reflect the impact more complex host-pathogen interactions can have on the host, nor the diversity in how immunity is regulated. Humans develop immune responses in the context of the periodic exposure to multiple pathogens and vaccines over a life-time. These are likely to have a long-lasting effect on who and what we are and how we respond to further antigen challenge. Therefore, studies on how infection influences immune homeostasis and how the development of responses to a pathogen reflects what is known on immune regulation will be informative on how we can translate findings from our standard models into treatments usable in humans.

One organism allows us to do just this. Bacteria of the genus Salmonella are devastating human pathogens. Nevertheless, many aspects of the diseases they cause can be successfully modelled in murine systems so that the infection is either resolving or non-resolving. This has the advantage of allowing the long-term impact of infection on immune function to be assessed. We propose to welcome key workers to write about their research that examine the consequence of Salmonella infection on the host and the elements of the bacterium that contribute to this.

This book discusses novel concepts and discoveries concerning the regulation of innate immunity by autophagy and autophagy-related proteins. In the past decade, there have been major advances in our understanding of the molecular mechanisms of autophagy and its physiological functions. This book highlights emerging studies on the underlying mechanisms of autophagy regulation of innate immunity, including inflammation, antiviral immunity and anti-bacterial responses and the signaling pathways that prompt or inhibit the initiation and progression of related diseases. It also offers new ideas and strategies for future drugs based on manipulating autophagy, especially selective autophagy mediated by cargo receptors. Providing a comprehensive overview of the autophagy regulation of innate immunity, it is a valuable resource for graduate students and researchers in the fields of immunology, cell biology and translational medicine.

The discovery of Toll-like receptors (TLRs) in the late 1990s ushered in a new age of discovery for innate immunity. The importance of TLRs for immunology and biomedical research was recognized with the Nobel Prize for Medicine or Physiology in 2011. The prize was shared by three scientists: Ralph Steinman (for the discovery of dendritic cells, whi