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This book highlights information derived primarily from clinical samples, with particular reference to theoretical and scientific aspects of the human immune system. This text will focus on topics that range from host-pathogen interactions in infectious disease to host immune response in cancer, allergic diseases, neuroinflammatory diseases, and autoimmune disorders. The reader will also have a well-rounded understanding of the behavior of the immune system with particular emphasis on the role of immunoproteomics in immunotherapy, neuroprotective immunity for neurodegenerative and neuroinfectious disease, leukemia-associated dendritic cell induction of adaptive immunity dysregulation, and the role of immune checkpoint inhibitors in cancer, infection, as well as neuroinflammation. Taken together, the contents of this book are intended for both clinicians and researchers in academia and industry.
The 2e of the gold standard text in the field, Nonhuman Primates in Biomedical Research provides a comprehensive, up-to-date review of the use of nonhuman primates in biomedical research. The Diseases volume provides thorough reviews of naturally occurring diseases of nonhuman primates, with a section on biomedical models reviewing contemporary nonhuman primate models of human diseases. Each chapter contains an extensive list of bibliographic references, photographs, and graphic illustrations to provide the reader with a thorough review of the subject. - Fully revised and updated, providing researchers with the most comprehensive review of the use of nonhuman primates in bioledical research - Addresses commonly used nonhuman primate biomedical models, providing researchers with species-specific information - Includes four color images throughout
A successful vaccine for the prevention and/or immunotherapy against HIV/AIDS is one of the prominent challenges of the 21st century. To date, all human vaccine trials against this virus/disease have resulted in failure, or at best have shown very low efficacy. The scientific community dealing with HIV/AIDS has unanimously proposed a focus on basic science, with the intention of identifying correlates of protection that can serve as guides in developing and evaluating vaccine preparation. However, Nature seems to have already found several ways of dealing with infections by HIV and related primate lentiviruses, either by resisting infection or, once infected, avoiding immune damage and immunodeficiency. Models of Protection Against HIV/SIV will allow for an in-depth reflection on the perspectives for vaccine and therapy research derived from important recent studies. It will be authored by some of the most well known specialists in the field of HIV resistance/protection: including F. Barré-Sinoussi (2008 Nobel Prize for Medicine winner), B. Walker, S. Rowland-Jones, A. Telenti, M. Lederman and F. Plummer. This book is structured in a unique way, looking at three models of resistance/protection separately and then comparing the models against one another to provide its readership with a detailed examination of the research that is most predominant in the search for a vaccine. This structure presents the information in an easy-to-understand format and gives the book a cross-discipline appeal -- an important reference for those in the scientific community, medical care, public health and academia alike. Provides extensive descriptions and comparisons on the different models of protection agains HIV/AIDS Comprehensive writing and illustrations Contributors are among the most eminent specialists in the field
The past few years have witnessed an explosive increase in our collective knowledge of the biology of the human immunodeficiency virus (HIV). Researchers have acquired new understanding of the virus's biochemistry, molecular biology, pathogenesis, genetics, and immunobiology. Resulting therapeutic advances have significantly prolonged the lives of thousands. Yet, the need to develop better therapies is ever more acute and--given the virus's continued spread through the human population--the need for an effective vaccine is urgent. These goals can be accomplished only through the experienced synthesis of information from the many disciplines participating in HIV research and through the insights of new investigators. This volume is designed to lower the barriers imposed on investigators by the sheer volume of available information--information that often can be found only in far-flung and specialized journals. It provides, in a single resource, an in-depth overview of the diverse areas that constitute HIV research. The result is a broad introduction for students and researchers new to the field as well as an integrated overview for researchers specialized in particular areas of HIV investigation. The volume will also benefit those seeking technical understanding of the virus's biology, including physicians treating HIV-infected patients. Each chapter is a comprehensive presentation of one area of current AIDS research--including work on the virus life cycle, epidemiology, genetics, protease and reverse transcriptase inhibitors, receptor and co-receptor interactions, therapeutic targets, clinical treatment, immunobiology, and vaccines--written by a leading researcher in that area. The contributors are Jon P. Anderson, Jan Balzarini, Elana Cherry, Thomas J. Coates, Chris Collins, Jon H. Condra, Mark B. Feinberg, Richard B. Gaynor, Matthias Götte, Daria J. Hazuda, Spyros Kalams, Nathaniel R. Landau, Gerald H. Learn, Norman L. Letvin, James I. Mullins, Willscott E. Naugler, David Nickle, Matthew Rain, Allen G. Rodrigo, Daniel Shriner, Shalom Spira, Mario Stevenson, Todd Summers, Catherine Ulich, Joseph P. Vacca, Mark A. Wainberg, Bruce D. Walker, and Yang Wang.
This comprehensive, authoritative treatise covers all aspects of mucosal vaccines including their development, mechanisms of action, molecular/cellular aspects, and practical applications. The contributing authors and editors of this one-of-a-kind book are very well known in their respective fields. Mucosal Vaccines is organized in a unique format in which basic, clinical, and practical aspects of the mucosal immune system for vaccine development are described and discussed. This project is endorsed by the Society for Mucosal Immunology. - Provides the latest views on mucosal vaccines - Applies basic principles to the development of new vaccines - Links basic, clinical, and practical aspects of mucosal vaccines to different infectious diseases - Unique and user-friendly organization
Dendritic cells are key players during HIV pathogenesis, and shape both the immediate immune response at the site of infection as well as directing the adaptive immune response against the virus. HIV has developed a plethora of immune evasion mechanisms that hijack dendritic cell functions, suppressing their ability to mount an accurate immune response and exploiting them for efficient viral transfer to target T cells. To achieve successful replication within dendritic cells without triggering danger signaling, HIV accomplishes a delicate balance where only a low level of transcription can be sustained without triggering antiviral responses that would harm the virus. Here, we describe how the presence of HSV2 coinfection, which is very common in geographic areas with a high HIV prevalence and almost triples the risk of HIV acquisition, alters dendritic cell state to support much higher levels of HIV infection. We found this effect to be mediated by the STING pathway, which is involved in the sensing of DNA in the cell cytosol. STING activation led to an upregulation of factors such as IRF3 and NFkB that can be used for HIV transcription and a degradation of factors that restrict HIV replication. In addition, we describe how HIV exploits the human complement system, a group of proteins that usually help the human body to identify dangerous pathogens while avoiding reaction towards self. HIV can coat itself, i.e. become opsonized, in complement fragments that are typically only present on the body’s own cells, allowing it to activate signaling pathways that are associated with tolerance. Dendritic cells that come into contact with complement opsonized HIV do not mount danger responses, despite the fact that HIV-derived single stranded RNA triggers the pathogen recognition receptor TLR8. The suppression of danger responses is mediated by activation of complement receptor 3, and leads to an increased infection of the dendritic cell and affects its interactions with other immune cells. There is a lack of recruitment of NK cells to the site of infection, and an inhibition of NK cell killing, which plays an important role in the destruction of HIV-infected cells in vivo. T cells primed by dendritic cells exposed to complement opsonized HIV have a lower ability to develop towards effector phenotype, and have an increased expression of the markers PD1, TIM3 and LAG3 which are associated with T cell dysfunction and exhaustion. In addition, T cells primed by these dendritic cells in the presence of NK cells upregulate markers CD38, CXCR3 and CCR4, which have been linked to an increased susceptibility to HIV infection. In summary, we add to the current knowledge on HIV immune evasion mechanisms that allow the virus to establish infection, as well as describing mechanisms that govern whether dendritic cells mount danger signaling and an immune response or not.