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Long-lasting T cell immunity is delivered by an array of individual T lymphocytes expressing clonally distributed and highly specific antigen receptors recognizing an almost infinite number of antigens that might enter in contact with the host. Following antigen-specific priming in lymphnodes, naïve CD4 and CD8 T lymphocytes proliferate generating clones of effector cells that migrate to peripheral tissues and deliver unique antigen-specific effector functions. Moreover, a proportion of these effector lymphocytes survive as memory T cells that can be rapidly mobilized upon new exposure to the same antigen, even years after their primary induction. Innate immune cells play crucial roles in the induction and maintenance of this efficient protection system. Following the seminal discovery of Steinman and Cohen in 1974 describing a rare cell type capable of initiating antigen-specific responses in lymphnodes, Dendritic Cells (DC) have taken up the stage for several decades as professional Antigen Presenting Cells (APC). Although DC possess all attributes to prime naïve T lymphocytes, other immune cell subsets become crucial accessory cells during secondary and even primary activation. For instance, Monocytes (Mo) are rapidly recruited to inflammatory sites and have recently been recognized as capable of shaping T cell immunity, either directly through Ag presentation, or indirectly through the secretion of soluble factors. In addition, upon sensing of T cell-derived cytokines, Mo differentiate into functionally different APC types that further impact on the quality and persistence of memory T cell responses in peripheral tissues. Other innate immune cells, including Myeloid Derived Suppressor Cells, Granulocytes and iNKT lymphocytes, are known to modulate T cell activation by interacting with and modifying the function of professional APC. Notably, innate immune cell determinants also account for the tissue-specific regulation of T cell immunity. Hence, the newly discovered family of Innate Lymphoid Cells, has been recognized to shape CD4+ T cell responses at mucosal surfaces. Although the actions of innate immune cells fulfills the need of initiating and maintaining protective T cell responses, the excessive presence or activity of individual determinants may be detrimental to the host, because it could promote tissue destruction as in autoimmunity and allergy, or conversely, prevent the induction of immune responses against malignant tissues, and even modulate the response to therapeutic agents. Thus, understanding how defined innate immune cell subsets control T cell immunity is of fundamental relevance to understand human health, and of practical relevance for preventing and curing human diseases. In this research topic, we intend to provide an excellent platform for the collection of manuscripts addressing in depth how diverse innate immune cell subsets impact on T cell responses through molecularly defined pathways and evaluating the rational translation of basic research into clinical applications.

Immunedeficiencies --- Antigen Presentation --- Granulocytes --- T cell memory --- Immunotherapy --- Skin --- Mononuclear Phagocytes --- innate lymphoid cells --- Inflammatory diseases --- Cancer

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The postprandial period is the metabolic phase that directly follows the ingestion of a meal. This period is critical to the handling of nutrients to feed the body throughout the whole day but it is also a time of challenge for the body’s metabolism, which has to be flexible and adaptable regarding the quantity and the quality of the nutrient intake. Changes in postprandial metabolism have been considered to be potential early markers in the pathophysiological course, finally leading to an increased risk of disease development. This book aimed to broaden and add to the research on the importance of postprandial metabolism in nutrition. The book includes literature reviews that cover the broad state of the art of our knowledge about postprandial metabolism, fine original studies of the complex changes in metabolism, and the physiological processes that are considered to drive the onset of pathogenesis. Finally, a series of examples on how nutrient content (especially proteins, sucrose, and lipids) can influence the postprandial metabolism over a wide range of phenomena operating during the postprandial period and how they could contribute to tipping the body towards adverse health processes.

peripheral blood mononuclear cells --- postprandial metabolism --- high fat–high sugar diet --- minipig --- adipose tissue --- biomarkers --- glucose --- human --- night --- postprandial --- wheat albumin --- energy expenditure --- fat oxidation --- respiratory quotient --- sucrose overfeeding --- hepatic steatosis --- intramyocellular lipids --- intrahepatocellular lipids --- dietary protein content --- dietary fat content --- plasma triglyceride --- liver --- gut --- obesity --- amino acid --- lactate --- nutrient flux --- short chain fatty acid --- aging --- catabolic state --- anabolic resistance --- protein synthesis --- energy bolus --- postprandial lipemia --- coconut oil --- butter --- canola oil --- olive oil --- lipid --- triglycerides --- dietary fat --- saturated fat --- cardiovascular disease --- carbohydrates --- cholesterol --- fibers --- food structure --- lipids --- polyphenols --- proteins --- vitamins --- ADMA --- arginine --- SDMA --- DMA --- PRMT --- alpha-glucosidase inhibitor --- biopeptides --- blood glucose --- glycemic control --- hyperglycemia --- milk peptides --- prediabetes --- pre-meal --- type 2 diabetes --- metabolic syndrome --- endothelial function --- oxidative stress --- nuts --- berries --- LBP --- sCD14 --- postprandial kinetics --- high-fat diet

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Dear Colleagues, The brain is vulnerable to injury. Following injury in the brain, apoptosis or necrosis may occur easily, leading to various functional disabilities. Neuronal death is associated with a number of neurological disorders including hypoxic ischemia, epileptic seizures, and neurodegenerative diseases. The brain subjected to injury is regarded to be responsible for the alterations in neurotransmission processes, resulting in functional changes. Oxidative stress produced by reactive oxygen species has been shown to be related to the death of neurons in traumatic injury, stroke, and neurodegenerative diseases. Therefore, scavenging or decreasing free radicals may be crucial for preventing neural tissues from harmful adversities in the brain. Neurotrophic factors, bioactive compounds, dietary nutrients, or cell engineering may ameliorate the pathological processes related to neuronal death or neurodegeneration and appear beneficial for improving neuroprotection. As a result of neuronal death or neuroprotection, the brain undergoes activity-dependent long-lasting changes in synaptic transmission, which is also known as functional plasticity. Neuroprotection implying the rescue from neuronal death is now becoming one of global health concerns. This Special Issue attempts to explore the recent advances in neuroprotection related to the brain. This Special Issue welcomes original research or review papers demonstrating the mechanisms of neuroprotection against brain injury using in vivo or in vitro models of animals as well as in clinical settings. The issues in a paper should be supported by sufficient data or evidence. Prof. Bae Hwan Lee Guest Editor

global cerebral ischemia --- amiloride --- sodium–hydrogen exchanger-1 --- zinc --- neuronal death --- neuroprotection --- neurodegenerative disorder --- choline acetyltransferase (ChAT) --- trimethyltin (TMT) --- bean phosphatidylserine (Bean-PS) --- brain-derived neurotrophic factor --- moderate hypoxia --- physical exercise --- psychomotor function --- reaction time --- cortisol --- catecholamines --- nitrite --- endotheline-1 --- lactate --- pyridoxine deficiency --- ischemia --- gerbil --- homocysteine --- cell death --- glia --- neurogenesis --- N-acetyl-l-cysteine --- transient receptor potential melastatin 2 --- neurodegeneration --- Alzheimer’s disease --- metabolic disease --- adiponectin --- insulin --- antioxidants --- stroke --- preventive gene therapy --- adenoviral vector --- VEGF --- GDNF --- NCAM --- human umbilical cord blood mononuclear cells --- antioxidant --- brain --- neurodegenerative disease --- oxidative stress --- PGC-1α --- vascular endothelial growth factor --- vascular endothelial growth factor receptor 2 --- PI3K/AKT --- MEK/ERK --- status epilepticus --- hippocampus --- middle cerebral artery occlusion --- reperfusion injury --- lipid emulsion --- excitotoxicity --- apoptosis --- GPR4 receptor --- MPP+ --- Parkinson’s disease --- CRISPR/cas9 --- ischemic stroke --- blood brain barrier --- nanoparticle-based drug delivery --- brain targeting --- BDNF --- miRNAs --- synaptic plasticity --- depression --- glioblastoma --- astrocytes --- astrocytic networks --- connexin 43 --- calcium activity --- neural injury --- nimodipine --- subarachnoid haemorrhage --- acid-sensing ion channels --- oxygen-glucose deprivation --- liver growth factor --- inflammation --- microglia --- Tg2576 transgenic mice --- amyloid-beta --- oculomotor system --- trophic factors --- motoneurons --- axotomy --- amyotrophic lateral sclerosis --- electroneutral transport --- cation-chloride cotransporters --- KCCs --- NKCCs --- WNK-SPAK/OSR1 --- ascorbic acid --- aging --- organotypic hippocampal slice culture --- n/a --- sodium-hydrogen exchanger-1 --- Alzheimer's disease --- Parkinson's disease