Macrophages In The Human Body

Through recent research, there has been a significant number of findings involving the biology of macrophages. Beyond the 1st line of defense, macrophages have several specific characteristics across different tissues, organs, and systems. Macrophages comprehend a heterogeneous phagocytic population with wide range phenotypes, and tissue-specific functions, such as bone resorption, extracellular matrix production, red blood cells and bacteria removal, among others. Through innate immune receptors macrophages can modulate several pathways that culminate in the production of various types of inflammatory mediators such as chemokines, cytokines, oxygen reactive species, and lipid mediators which ultimately altered the behavior of other cells. Moreover, environment signals modify and induce metabolic reprograming that it alters phenotype and functions.Macrophages in the Human Body: A Tissue Level Approach presents a current overview of the diversity of macrophages across multiple human body systems, their phenotype, function and metabolic characteristics. It covers translational aspects where there is research support to indicate the therapeutic potential. Covers translational aspects where there is research support to indicate potential therapeutic potential Aims at presenting a current overview of the diversity of macrophages across multiple human body systems, their phenotype, function and metabolic characteristics Introduces Macrophages generally and dive into the organ/tissue/specific representations covering their phenotype, function, and metabolic characteristics Brings updated aspects of macrophages biology

The Janeway's Immunobiology CD-ROM, Immunobiology Interactive, is included with each book, and can be purchased separately. It contains animations and videos with voiceover narration, as well as the figures from the text for presentation purposes.

This authoritative handbook covers all aspects of immunosenescence, with contributions from experts in the research and clinical areas. It examines methods and models for studying immunosenescence; genetics; mechanisms including receptors and signal transduction; clinical relevance in disease states including infections, autoimmunity, cancer, metabolic syndrome, neurodegenerative diseases, frailty and osteoporosis; and much more.

Monocytes represent one of the major types of white blood cells in man which prevent infection by ingesting and killing invading pathogens and by releasing factors which stimulate and regulate lymphocytes. Monocytes "purify" the blood, removing immune complexes, mediating inflammatory responses, and initiating tissue repair. Human Monocytes represents an up-to-date, definitive account of this important cell. It covers the cells biochemical, immunological, and inflammatory functionsand its role in many diseases, including asthma, atherosclerosis, rheumatoid arthritis, and AIDS.

Biology of the Lymphokines discusses the scope and diversity of lymphokine research. This book focuses on the studies on lymphokines, such as those involving cellular source, chemical nature, purification strategies, and bioassay limitations. The mechanism of lymphokine action, lymphokines in vivo, and value of lymphokine quantitations are also covered. This text describes the repertoire of lymphokines produced by various lymphoblastoid cell lines and its significance for coping with the problem of large scale lymphokine production. The anti-viral and general immunoregulatory properties of interferons and rationale developed for integrating interferons with the family of lymphokines are likewise deliberated. This publication is a good source for students and researchers conducting work on lymphokines.

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 micro environmental 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 provide state-of-the art knowledge of these cells in health and disease.

The inflammasome was first described in 2002 as a molecular complex activating proinflammatory caspases and therefore regulating the maturation and biological activities of cytokines such as IL-1 and IL-18. This finding was substantiated by the identification of several mutations in the cias1 gene, encoding the human NLRP3 protein, responsible for several autoinflammatory disorders such as the Muckle Wells syndrome. Since, the interest for this complex has constantly increased and several inflammasome complexes with different specificities have been described. These inflammasomes sense a wide variety of pathogens and danger signals and are key players in the inflammatory response. With the contributions of leading international experts in the field, this book provides an extensive overview of the current knowledge of inflammasome biology and their role in health and disease.

This book provides up-to-date information on the crucial interaction of pathogenic bacteria and professional phagocytes, the host cells whose purpose is to ingest, kill, and digest bacteria in defense against infection. The introductory chapters focus on the receptors used by professional phagocytes to recognize and phagocytose bacteria, and the signal transduction events that are essential for phagocytosis of bacteria. Subsequent chapters discuss specific bacterial pathogens and the strategies they use in confronting professional phagocytes. Examples include Helicobacter pylori, Streptococcus pneumoniae, and Yersinae, each of which uses distinct mechanisms to avoid being phagocytosed and killed. Contrasting examples include Listeria monocytogenes and Mycobacterium tuberculosis, which survive and replicate intracellularly, and actually cooperate with phagocytes to promote their entry into these cells. Together, the contributions in this book provide an outstanding review of current knowledge regarding the mechanisms of phagocytosis and how specific pathogenic bacteria avoid or exploit these mechanisms.

Macrophages have unique and diverse functions necessary for survival. And, in humans (and other species), they are the most abundant leukocytes in tissues. The Innate functions of macrophages that are best known are their unusual ability to either “Kill” or “Repair”. Since killing is a destructive process and repair is a constructive process, it was stupefying how one cell could exhibit these 2 polar – opposite functions. However, in the late 1980’s, it was shown that macrophages have a unique ability to enzymatically metabolize Arginine to Nitric Oxide (NO, a gaseous non – specific killer molecule) or to Ornithine (a precursor of polyamines and collagen for repair). The dual Arginine metabolic capacity of macrophages provided a functional explanation for their ability to kill or repair. Macrophages predominantly producing NO are called M1 and those producing Ornithine are called M2. M1 and M2 – dominant responses occur in lower vertebrates, and in T cell deficient vertebrates being directly driven by Damage and Pathogen Associated Molecular Patterns (DAMP and PAMP). Thus, M1 and M2 are Innate responses that protect the host without Adaptive Immunity. In turn, M1/M2 is supplanting previous models in which T cells were necessary to “activate” or “alternatively activate” macrophages (the Th1/Th2 paradigm). M1 and M2 macrophages were named such because of the additional key findings that these macrophages stimulate Th1 and Th2 – like responses, respectively. So, in addition to their unique ability to kill or repair, macrophages also govern Adaptive Immunity. All of the foregoing would be less important if M1 or M2 – dominant responses were not observed in disease. But, they are. The best example to date is the predominance of M2 macrophages in human tumors where they act like wound repair macrophages and actively promote growth. More generally, humans have become M2 – dominant because sanitation, antibiotics and vaccines have lessened M1 responses. And, M2 dominance seems the cause of ever - increasing allergies in developed countries. Obesity represents a new and different circumstance. Surfeit energy (e.g., lipoproteins) causes monocytes to become M1 dominant in the vessel walls causing plaques. Because M1 or M2 dominant responses are clearly causative in many modern diseases, there is great potential in developing the means to selectively stimulate (or inhibit) either M1 or M2 responses to kill or repair, or to stimulate Th1 or Th2 responses, depending on the circumstance. The contributions here are meant to describe diseases of M1 or M2 dominance, and promising new methodologies to modulate the fungible metabolic machinery of macrophages for better health.