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The immune system detects "danger" through a series of what we call pathogen-associated molecular patterns (PAMPs) or damage-associated molecular pattern molecules (DAMPs), working in concert with both positive and negative signals derived from other tissues. PAMPs are molecules associated with groups of pathogens that are small molecular motifs conserved within a class of microbes. They are recognized by Toll-like receptors (TLRs) and other pattern recognition receptors. A vast array of different types of molecules can serve as PAMPs, including glycans and glycoconjugates. Bacterial lipopolysaccharides (LPSs), endotoxins found on the cell membranes of Gram-negative bacteria, are considered to be the prototypical class of PAMPs. LPSs are specifically recognized by TLR4, a recognition receptor of the innate immune system. Other PAMPs include bacterial flagellin (recognized by TLR5), lipoteichoic acid from Gram-positive bacteria, peptidoglycan, and nucleic acid variants normally associated with viruses, such as double-stranded RNA, recognized by TLR3 or unmethylated CpG motifs, recognized by TLR9. DAMPs, also known as alarmins, are molecules released by stressed cells undergoing necrosis that act as endogenous danger signals to promote and exacerbate the immune and inflammatory response. DAMPs vary greatly depending on the type of cell (epithelial, mesenchymal, etc.) and injured tissue. Some endogenous danger signals include heat-shock proteins, HMGB1 (high-mobility group box 1), reactive oxygen intermediates, extracellular matrix breakdown products such as hyaluronan fragments, neuromediators, and cytokines like the interferons (IFNs). Non-protein DAMPs include ATP, uric acid, heparin sulfate, and DNA. Furthermore, accumulating evidence supports correlation between alarmins and changes in the microbiome. Increased serum or plasma levels of these DAMPs have been associated with many inflammatory diseases, including gastric and intestinal inflammatory diseases, graft-versus-host disease (GVHD), sepsis and multiple organ failure, allergies particularly in the lungs, atherosclerosis, age-associated insulin resistance, arthritis, lupus, neuro-inflammation/degeneration and more recently in tumors, which is particularly interesting with the emergence of immunotherapies. Therapeutic strategies are being developed to modulate the expression of these DAMPs for the treatment of these diseases. A vast number of reviews have already been published in this area; thus, in an effort to not duplicate what has already been written, we will focus on recent discoveries particularly in disease models that are epidemic in Western society: intestinal chronic inflammatory diseases including GVHD and its relationship with the microbiome, chronic infectious diseases, allergies, autoimmune diseases, neuroinflammation and cancers. We will also focus on the basic cellular roles of macrophages, T cells and B cells. This research topic brings together sixteen articles that provide novel insights into the mechanisms of action of DAMPS/alarmins and their regulation and subsequent immunologically driven responses.

Diseases --- Molecular immunology. --- Molecular aspects. --- damage-associated molecular pattern molecules (DAMPs) --- pathogen-associated molecular patterns (PAMPs) --- inflammation --- immune cells --- alarmins

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This book outlines some new advances in genetics, clinical evaluation, localization, therapy (newly including immunotherapy) of pheochromocytoma and paraganglioma including their metastatic counterparts. Well-known and experienced clinicians and scientists contributed to this book to include some novel approaches to these tumors. This book will serve to various health care professionals from different subspecialties, but mainly oncologists, endocrinologists, endocrine surgeons, pediatricians, and radiologists. This book shows that the field of pheochromocytoma/paraganglioma is evolving and a significant progress has been made in last 5 years requiring that health care professionals and scientists will learns new information and implement it in their clinical practice or scientific work, respectively. This book should not be missed by anybody who is focusing on neuroendocrine tumors, their newest evaluation and treatment.

polycythemia --- peptide receptor radiotherapy --- n/a --- vasculogenesis --- catecholamines --- neuroendocrine --- GTV --- adaptive immunity --- therapy resistance --- histology --- transgenic mice --- cryoablation --- spheroids --- energy metabolism --- somatostatinoma --- angiogenesis --- pheochromocytoma --- SDHD --- percutaneous ethanol injection --- metanephrines --- SDHB --- global longitudinal strain --- mutation --- normetanephrines --- catecholamine --- PASS --- PGL --- 177Lu-DOTATATE --- chromosomal alteration --- speckle-tracking echocardiography --- lL-6 --- dog --- percutaneous ablation --- stem-like tumor cells --- EPAS1 --- neural crest --- fluorescence imaging --- neutrophil --- xenograft --- inflammation --- head and neck --- weighted standard deviation --- FGF21 --- calorimetry --- HIF --- average real variability --- next-generation sequencing --- adrenocortical carcinoma --- carotid body --- hypoxia-inducible factor --- paraganglioma --- succinate dehydrogenase --- blood pressure variability --- arrhythmia --- mortality --- NF1 --- toll-like receptor --- GAPP --- NET --- subclinical systolic dysfunction --- pheochromocytoma and paraganglioma --- PET-CT --- pan-cancer analysis --- mouse pheochromocytoma cells --- innate immunity --- neurogenesis --- neuroendocrine tumor --- obesity --- hypotension --- hypoxia --- CNV detection --- 18F-FDOPA --- comparative genomics --- adrenomedullary function --- PCC --- pathogen-associated molecular patterns --- adrenal tumor --- radiotherapy --- 11C-hydroxy-ephedrine --- radiofrequency ablation --- PPGL --- minimally invasive procedure --- sporadic --- diabetes mellitus --- adrenal incidentaloma --- germline mutation --- immunotherapy --- VHL --- immunohistochemistry --- metastatic OR malignant pheochromocytoma --- erythropoietin --- postoperative --- targeted therapy --- PRRT --- metastatic --- mitochondria --- T cell --- TCA cycle --- meta-analysis --- pseudohypoxia --- ectopic secretion --- radiosensitization --- chromogranin A --- hereditary --- hypertension --- PET --- phosphorylation tyrosine hydroxylase