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The mononuclear phagocyte system (MPS) comprises dendritic cells (DCs), monocytes and macrophages (MØs) that together play crucial roles in tissue immunity and homeostasis, but also contribute to a broad spectrum of pathologies. They are thus attractive therapeutic targets for immune therapy. However, the distinction between DCs, monocytes and MØ subpopulations has been a matter of controversy and the current nomenclature has been a confounding factor. DCs are remarkably heterogeneous and consist of multiple subsets traditionally defined by their expression of various surface markers. While markers are important to define various populations of the MPS, they do not specifically define the intrinsic nature of a cell population and do not always segregate a bona fide cell type of relative homogeneity. Markers are redundant, or simply define distinct activation states within one subset rather than independent subpopulations. One example are the steady-state CD11b+ DCs which are often not distinguished from monocytes, monocyte-derived cells, and macrophages due to their overlapping phenotype. Lastly, monocyte fate during inflammation results in cells bearing the phenotypic and functional features of both DCs and MØs significantly adding to the confusion. In fact, depending on the context of the study and the focus of the laboratory, a monocyte-derived cell will be either be called "monocyte-derived DCs" or "macrophages". Because the names we give to cells are often associated with a functional connotation, this is much more than simple semantics. The "name" we give to a population fundamentally changes the perception of its biology and can impact on research design and interpretation. Recent evidence in the ontogeny and transcriptional regulation of DCs and MØs, combined with the identification of DC- and MØ-specific markers has dramatically changed our understanding of their interrelationship in the steady state and inflammation. In steady state, DCs are constantly replaced by circulating blood precursors that arise from committed progenitors in the bone marrow. Similarly, some MØ populations are also constantly replaced by circulating blood monocytes. However, others tissue MØs are derived from embryonic precursors, are seeded before birth and maintain themselves in adults by self-renewal. In inflammation, such differentiation pathways are fundamentally changed and unique monocyte-derived inflammatory cells are generated. Current DC, monocyte and MØ nomenclature does not take into account these new developments and as a consequence is quite confusing. We believe that the field is in need of a fresh view on this topic as well as an upfront debate on DC and MØ nomenclature. Our aim is to bring expert junior and senior scientists to revisit this topic in light of these recent developments. This Research Topic will cover all aspects of DC, monocyte and MØ biology including development, transcriptional regulation, functional specializations, in lymphoid and non-lymphoid tissues, and in both human and mouse models. Given the central position of DCs, monocytes and MØs in tissue homeostasis, immunity and disease, this topic should be of interest to a large spectrum of the biomedical community.

Dendritic cells --- Macrophages --- Nomenclature. --- nomenclature --- Monocytes --- development --- Dendritic Cells --- Subset --- differentiation --- Antigen Presentation --- Mononuclear Phagocyte System --- Ontogeny

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Inflammation. --- Macrophages. --- Histiocytes --- Mononuclear phagocytes --- Antigen presenting cells --- Connective tissue cells --- Killer cells --- Phagocytes --- Reticulo-endothelial system --- Inflammatory process --- Pathology --- Anti-inflammatory agents

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Macrophages are tissue resident phagocytes that have important roles in development and immunity. The observation that cancers become infiltrated by large numbers of macrophages was first made by Virchow in 1863, clinical and experimental studies suggest tumor-associated macrophages (TAM) are critical to promote carcinogenesis and tumor-progression, however to this day it still isn’t clear what regulates the recruitment of macrophages in tumors and what drives their pro-tumor functions. This volume will provide an overview of current research on the form and function of TAM, highlighting both the mechanistic roles they play in carcinogenesis and tumor progression as well as the molecular mechanisms that control their phenotype and function, and the final chapter addresses the issue of TAM as a potential target in cancer therapy.

Cancer -- Research. --- Macrophages. --- Tumors. --- Macrophages --- Tumors --- Immunology --- Cancer --- Disease Attributes --- Mononuclear Phagocyte System --- Phagocytes --- Connective Tissue Cells --- Myeloid Cells --- Diseases --- Cells --- Immune System --- Pathologic Processes --- Anatomy --- Pathological Conditions, Signs and Symptoms --- Hemic and Immune Systems --- Neoplasms --- Disease Progression --- Biology --- Medicine --- Health & Biological Sciences --- Oncology --- Microbiology & Immunology --- Growth --- Immunological aspects --- Tumours --- Histiocytes --- Mononuclear phagocytes --- Medicine. --- Cancer research. --- Pharmacology. --- Biomedicine. --- Cancer Research. --- Pharmacology/Toxicology. --- Pathology --- Cysts (Pathology) --- Antigen presenting cells --- Connective tissue cells --- Killer cells --- Reticulo-endothelial system

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Macrophages are a key component of the innate immune system and play an integral role in host defense and homeostasis. On one hand, these cells contribute to host defence by triggering inflammation, displaying microbicidal/tumoricidal properties, regulating the activation of adaptive immunity and promoting resolution of inflammation. On the other hand, they contribute to essential trophic functions such as neural patterning, bone morphogenesis and ductal branching in mammary glands. Thus, macrophages are extremely versatile cells that can respond efficiently to tissue microenvironmental cues by polarizing to distinct phenotypes, depending on the functions they need to perform. Indeed, functional diversity and plasticity are hallmarks of these cells. Macrophages may also play a detrimental role. An overwhelming body of literature has indicated their crucial role in pathogenesis. The list includes sepsis, cancer, metabolic syndrome, immunodeficiency, auto-immune disease- virtually impacting every major pathology that we know. These observations have suggested macrophages and their related molecules as potential targets in therapeutic applications. Available evidence proclaims macrophages as a key player in homeostasis, host defense and disease. Crucial developments in the past few years call for a re-evaluation and update of our understanding of macrophages. The present book is an endeavour that attempts to provide state-of-the art knowledge of these cells in health and disease.

Macrophages. --- Histiocytes --- Mononuclear phagocytes --- Antigen presenting cells --- Connective tissue cells --- Killer cells --- Phagocytes --- Reticulo-endothelial system --- Immunology. --- Monoclonal antibodies. --- Microbiology. --- Antibodies. --- Medical Microbiology. --- Microbial biology --- Biology --- Microorganisms --- Antibodies, Monoclonal --- Monoclonal immunoglobulins --- Immunoglobulins --- Molecular cloning --- Immunobiology --- Life sciences --- Serology --- Medical microbiology. --- Antibodies --- Immune globulins --- Immune serum globulin --- Blood proteins --- Globulins --- Plasma cells --- Antibody diversity --- Antigens --- Bacterial immunoglobulin-binding proteins

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Macrophages are core components of the innate immune system. Once activated, they may have either pro- or anti-inflammatory effects that include pathogen killing, safe disposal of apoptotic cells or tissue renewal. The activation state of macrophages is conceptualized by the so-called M1/M2 model of polarization. M2 macrophages are not simply antagonists of M1 macrophages; rather, they represent a network of tissue resident macrophages with roles in tissue development and organ homeostasis. M2 macrophages govern functions at the interfaces of immunity, tissue development and turnover, metabolism, and endocrine signaling. Dysfunction in M2 macrophages can ruin the healthy interplay between the immune system and metabolic processes, and lead to diseases such as insulin resistance, metabolic syndrome, and type 1 and 2 diabetes mellitus. Furthermore, M2 macrophages are essential for healthy tissue development and immunological self-tolerance. Worryingly, these functions of M2 macrophages can also be disrupted, resulting in tumor growth and autoimmunity. This book comprehensively discusses the biology of M2 macrophages, summarizes the current state of knowledge, and highlights key questions that remain unanswered.

Immunology. --- Cell biology. --- Lipids. --- Infectious diseases. --- Human physiology. --- Cell Biology. --- Lipidology. --- Infectious Diseases. --- Human Physiology. --- Human biology --- Medical sciences --- Physiology --- Human body --- Lipides --- Lipins --- Lipoids --- Biomolecules --- Steroids --- Cell biology --- Cellular biology --- Biology --- Cells --- Cytologists --- Immunobiology --- Life sciences --- Serology --- Macrophages. --- Histiocytes --- Mononuclear phagocytes --- Antigen presenting cells --- Connective tissue cells --- Killer cells --- Phagocytes --- Reticulo-endothelial system --- Communicable diseases. --- Infection.