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Obesity and its co-morbidities, including atherosclerosis, insulin resistance and diabetes, are a world-wide epidemic. Inflammatory immune responses in metabolic tissues have emerged as a universal feature of these metabolic disorders. While initial work highlighted the contribution of macrophages to tissue inflammation and insulin resistance, recent studies demonstrate that cells of the adaptive immune compartment, including T and B lymphocytes and dendritic cells also participate in obesity-induced pathogenesis of these conditions. However, the molecular and cellular pathways by which the innate and adaptive branches of immunity control tissue and systemic metabolism remain poorly understood. To engage in growth and activation, cells need to increase their biomass and replicate their genome. This process presents a substantial bioenergetic challenge: growing and activated cells must increase ATP production and acquire or synthesize raw materials, including lipids, proteins and nucleic acids. To do so, they actively reprogram their intracellular metabolism from catabolic mitochondrial oxidative phosphorylation to glycolysis and other anabolic pathways. This metabolic reprogramming is under the control of specific signal transduction pathways whose underlying molecular mechanisms and relevance to physiology and disease are subject of considerable current interest and under intense study. Recent reports have elucidated the physiological role of metabolic reprogramming in macrophage and T cell activation and differentiation, B- and dendritic cell biology, as well as in the crosstalk of immune cells with endothelial and stem cells. It is also becoming increasingly evident that alterations of metabolic pathways play a major role in the pathogenesis of chronic inflammatory disorders. Due to the scientific distance between immunologists and experts in metabolism (e.g., clinicians and biochemists), however, there has been limited cross-talk between these communities. This collection of articles aims at promoting such cross-talk and accelerating discoveries in the emerging field of immunometabolism.
metabolic syndrome --- Obesity --- Immunometabolism --- TCA cycle --- Glycolysis --- macrophage --- Inflammation --- fatty acid oxidation --- Pentose Phosphate Pathway --- lymphocyte
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This eBook is a collection of articles from a Frontiers Research Topic. Frontiers Research Topics are very popular trademarks of the Frontiers Journals Series: they are collections of at least ten articles, all centered on a particular subject. With their unique mix of varied contributions from Original Research to Review Articles, Frontiers Research Topics unify the most influential researchers, the latest key findings and historical advances in a hot research area! Find out more on how to host your own Frontiers Research Topic or contribute to one as an author by contacting the Frontiers Editorial Office: frontiersin.org/about/contact
immunometabolism --- metabolic reprogramming --- immune cell regulation --- cell fate decisions --- T cells --- myeloid cells --- innate lymphoid cells
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Obesity and its co-morbidities, including atherosclerosis, insulin resistance and diabetes, are a world-wide epidemic. Inflammatory immune responses in metabolic tissues have emerged as a universal feature of these metabolic disorders. While initial work highlighted the contribution of macrophages to tissue inflammation and insulin resistance, recent studies demonstrate that cells of the adaptive immune compartment, including T and B lymphocytes and dendritic cells also participate in obesity-induced pathogenesis of these conditions. However, the molecular and cellular pathways by which the innate and adaptive branches of immunity control tissue and systemic metabolism remain poorly understood. To engage in growth and activation, cells need to increase their biomass and replicate their genome. This process presents a substantial bioenergetic challenge: growing and activated cells must increase ATP production and acquire or synthesize raw materials, including lipids, proteins and nucleic acids. To do so, they actively reprogram their intracellular metabolism from catabolic mitochondrial oxidative phosphorylation to glycolysis and other anabolic pathways. This metabolic reprogramming is under the control of specific signal transduction pathways whose underlying molecular mechanisms and relevance to physiology and disease are subject of considerable current interest and under intense study. Recent reports have elucidated the physiological role of metabolic reprogramming in macrophage and T cell activation and differentiation, B- and dendritic cell biology, as well as in the crosstalk of immune cells with endothelial and stem cells. It is also becoming increasingly evident that alterations of metabolic pathways play a major role in the pathogenesis of chronic inflammatory disorders. Due to the scientific distance between immunologists and experts in metabolism (e.g., clinicians and biochemists), however, there has been limited cross-talk between these communities. This collection of articles aims at promoting such cross-talk and accelerating discoveries in the emerging field of immunometabolism.
metabolic syndrome --- Obesity --- Immunometabolism --- TCA cycle --- Glycolysis --- macrophage --- Inflammation --- fatty acid oxidation --- Pentose Phosphate Pathway --- lymphocyte
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Obesity and its co-morbidities, including atherosclerosis, insulin resistance and diabetes, are a world-wide epidemic. Inflammatory immune responses in metabolic tissues have emerged as a universal feature of these metabolic disorders. While initial work highlighted the contribution of macrophages to tissue inflammation and insulin resistance, recent studies demonstrate that cells of the adaptive immune compartment, including T and B lymphocytes and dendritic cells also participate in obesity-induced pathogenesis of these conditions. However, the molecular and cellular pathways by which the innate and adaptive branches of immunity control tissue and systemic metabolism remain poorly understood. To engage in growth and activation, cells need to increase their biomass and replicate their genome. This process presents a substantial bioenergetic challenge: growing and activated cells must increase ATP production and acquire or synthesize raw materials, including lipids, proteins and nucleic acids. To do so, they actively reprogram their intracellular metabolism from catabolic mitochondrial oxidative phosphorylation to glycolysis and other anabolic pathways. This metabolic reprogramming is under the control of specific signal transduction pathways whose underlying molecular mechanisms and relevance to physiology and disease are subject of considerable current interest and under intense study. Recent reports have elucidated the physiological role of metabolic reprogramming in macrophage and T cell activation and differentiation, B- and dendritic cell biology, as well as in the crosstalk of immune cells with endothelial and stem cells. It is also becoming increasingly evident that alterations of metabolic pathways play a major role in the pathogenesis of chronic inflammatory disorders. Due to the scientific distance between immunologists and experts in metabolism (e.g., clinicians and biochemists), however, there has been limited cross-talk between these communities. This collection of articles aims at promoting such cross-talk and accelerating discoveries in the emerging field of immunometabolism.
metabolic syndrome --- Obesity --- Immunometabolism --- TCA cycle --- Glycolysis --- macrophage --- Inflammation --- fatty acid oxidation --- Pentose Phosphate Pathway --- lymphocyte --- metabolic syndrome --- Obesity --- Immunometabolism --- TCA cycle --- Glycolysis --- macrophage --- Inflammation --- fatty acid oxidation --- Pentose Phosphate Pathway --- lymphocyte
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This eBook is a collection of articles from a Frontiers Research Topic. Frontiers Research Topics are very popular trademarks of the Frontiers Journals Series: they are collections of at least ten articles, all centered on a particular subject. With their unique mix of varied contributions from Original Research to Review Articles, Frontiers Research Topics unify the most influential researchers, the latest key findings and historical advances in a hot research area! Find out more on how to host your own Frontiers Research Topic or contribute to one as an author by contacting the Frontiers Editorial Office: frontiersin.org/about/contact
Medicine --- Immunology --- immunometabolism --- metabolic reprogramming --- immune cell regulation --- cell fate decisions --- T cells --- myeloid cells --- innate lymphoid cells --- immunometabolism --- metabolic reprogramming --- immune cell regulation --- cell fate decisions --- T cells --- myeloid cells --- innate lymphoid cells
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This eBook is a collection of articles from a Frontiers Research Topic. Frontiers Research Topics are very popular trademarks of the Frontiers Journals Series: they are collections of at least ten articles, all centered on a particular subject. With their unique mix of varied contributions from Original Research to Review Articles, Frontiers Research Topics unify the most influential researchers, the latest key findings and historical advances in a hot research area! Find out more on how to host your own Frontiers Research Topic or contribute to one as an author by contacting the Frontiers Editorial Office: frontiersin.org/about/contact
Medicine --- Immunology --- immunometabolism --- metabolic reprogramming --- immune cell regulation --- cell fate decisions --- T cells --- myeloid cells --- innate lymphoid cells
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This Special Issue of Cancers (Basel) is mainly dedicated to selecting papers from the talks given during the first Joint Meeting on Lung Cancer (JMLC) between the MD Anderson Cancer Center (Houston, Texas USA) and the Hospital University Federation (HUF) OncoAge (University Côte d’Azur, Nice, France) (Nice, September 2018). The central theme of JMLC is to discuss new advances and exchange ideas regarding lung cancer. Notably, the talks covered different topics on new therapeutic strategies (targeted therapy and immuno-oncology), molecular and cellular biology, biomarkers, and the epidemiology of lung cancer. Special attention was also given to lung cancer in elderly patients. The articles published in this Special Issue covered subjects such as the assessment of new biomarkers and new approaches for the early detection of lung cancer, epidemiological data, and emphasized a place for the newly characterized cellular pathways in lung cancer, which opens room for therapeutic perspectives for lung cancer patients.
microRNAs --- multiplexed --- screening --- education --- non-smoker --- image analysis --- artificial intelligence --- research --- lung cancer --- spatial analysis --- optimization --- fluorescence --- geriatric assessment --- geriatric interventions --- TNBC --- liquid biopsy --- non-small cell lung cancer --- integrated approaches --- well-being --- hormone-like action --- EGFR mutations --- reversal of EMT --- tumor plasticity --- immune profiling --- macrophage --- multiplexed methodologies --- targeted treatment --- techniques --- immune-oncology --- bioinformatics --- MALAT1 --- long non-coding RNAs --- CD8 T Cells --- personal medicine --- EGFR TKIs --- lncRNA --- hormones --- elderly --- interleukin-1? and immunometabolism --- chromogenic --- xenograft --- metastasis --- PD-1/PD-L1 checkpoint blockade --- immunotherapy --- molecular --- cancer tissues --- digital --- NSCLC --- immune blockade --- lung adenocarcinoma --- circulating tumor cells --- brightfield --- non-coding RNAs --- older adults --- cancer --- tumor microenvironment --- aging --- rational therapy
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This book explores the biology of the fungal pathogen Candida albicans, its interaction with the human host, and current research that seeks to identify new ways to combat the health risks posed by C. albicans infection.
Candida albicans --- acridine --- antifungal --- topoisomerase --- inhibitor --- candidiasis --- 1,3,4-oxadiazole --- drug discovery --- antifungal agents --- drug resistance --- toxicity --- biofilm --- invasive Candida infections --- invasive fungal infections --- antifungal prophylaxis --- newborns --- surgery --- neonatal surgery --- multivalency --- anti-adhesion glycoconjugates --- glycomimetics --- Candida --- C. albicans --- XCL1 --- metamorphic protein --- fold-switching protein --- antifungal peptide --- polymorphism --- hyphal morphogenesis --- hyphal activation --- signal transduction pathways --- cell cycle regulation --- sphingolipids --- myriocin --- fungal infections --- epigenetic --- yeast --- chromatin --- hyphae --- human fungal pathogen --- nutrient sensing --- amino acid metabolism --- proline catabolism --- mitochondria --- SPS-sensor --- nitrogen catabolite repression --- glucose repression --- immunometabolism --- metabolism --- macrophages --- epithelial cells --- glycolysis --- glucose --- moonlighting proteins --- n/a
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This book explores the biology of the fungal pathogen Candida albicans, its interaction with the human host, and current research that seeks to identify new ways to combat the health risks posed by C. albicans infection.
Research & information: general --- Biology, life sciences --- Microbiology (non-medical) --- Candida albicans --- acridine --- antifungal --- topoisomerase --- inhibitor --- candidiasis --- 1,3,4-oxadiazole --- drug discovery --- antifungal agents --- drug resistance --- toxicity --- biofilm --- invasive Candida infections --- invasive fungal infections --- antifungal prophylaxis --- newborns --- surgery --- neonatal surgery --- multivalency --- anti-adhesion glycoconjugates --- glycomimetics --- Candida --- C. albicans --- XCL1 --- metamorphic protein --- fold-switching protein --- antifungal peptide --- polymorphism --- hyphal morphogenesis --- hyphal activation --- signal transduction pathways --- cell cycle regulation --- sphingolipids --- myriocin --- fungal infections --- epigenetic --- yeast --- chromatin --- hyphae --- human fungal pathogen --- nutrient sensing --- amino acid metabolism --- proline catabolism --- mitochondria --- SPS-sensor --- nitrogen catabolite repression --- glucose repression --- immunometabolism --- metabolism --- macrophages --- epithelial cells --- glycolysis --- glucose --- moonlighting proteins --- Candida albicans --- acridine --- antifungal --- topoisomerase --- inhibitor --- candidiasis --- 1,3,4-oxadiazole --- drug discovery --- antifungal agents --- drug resistance --- toxicity --- biofilm --- invasive Candida infections --- invasive fungal infections --- antifungal prophylaxis --- newborns --- surgery --- neonatal surgery --- multivalency --- anti-adhesion glycoconjugates --- glycomimetics --- Candida --- C. albicans --- XCL1 --- metamorphic protein --- fold-switching protein --- antifungal peptide --- polymorphism --- hyphal morphogenesis --- hyphal activation --- signal transduction pathways --- cell cycle regulation --- sphingolipids --- myriocin --- fungal infections --- epigenetic --- yeast --- chromatin --- hyphae --- human fungal pathogen --- nutrient sensing --- amino acid metabolism --- proline catabolism --- mitochondria --- SPS-sensor --- nitrogen catabolite repression --- glucose repression --- immunometabolism --- metabolism --- macrophages --- epithelial cells --- glycolysis --- glucose --- moonlighting proteins
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The book is based on the Cancers journal Special Issue entitled “Immunotherapy, Tumor Microenvironment and Survival Signaling", and focuses on important problems concerning tumors and tumor microenvironment interactions, as well as novel immunotherapies such as CAR-T cell therapy. Immunotherapies have recently shown remarkable results in the treatment of cancer patients. However, there are still many questions that remain to be solved in regards to more effective therapies, such as the tumor heterogeneous profile, tumor microenvironment, and tumor survival epigenetic and genetic pathways, all of which make patients resistant to the presently available treatments for cancer. This book demonstrates different approaches to overcome the challenges faced by immunotherapies due to suppressive tumor microenvironments. This book includes 18 papers that can be divided into three chapters: 1. novel immunotherapies; 2. targeting tumor microenvironment and novel approaches; 3. targeting tumors and tumor microenvironment in different types of cancer.
Medicine --- Clinical & internal medicine --- Autophagy --- colorectal cancer --- immunotherapy --- tumor stroma --- tumor microenvironment --- immune checkpoint inhibitors --- chemotherapy --- tyrosine kinase inhibitors --- angiogenesis --- check point inhibitors --- programmed cell death protein 1 --- programmed cell death 1 ligand 1 --- cardiotoxicity --- lung metastasis --- CAR-T --- hypoxia --- tumor --- microenvironment --- CD19 --- BCMA --- cancer --- melanoma --- immune escape --- antigen loss --- chimeric antigen receptor --- electroporation --- lentivirus --- lentiviral transduction --- macrophages --- leukemia cells --- lytic peptides --- targeted therapy --- dendritic cells --- pathogenesis --- risk factors --- breast cancer --- resistance --- checkpoint --- targeted treatment --- personalized medicine --- pediatric solid tumors --- chimeric antigen receptors --- cancer vaccines --- oncolytic viral therapy --- immunomodulation --- DCLK1 --- tumor stem cells --- clonogenicity --- mitochondria --- mitochondrial transfer --- tunneling nanotubes --- triple-negative breast cancer --- immune checkpoint inhibitor --- combination therapy --- cancer nanomedicine --- tumor antigens --- cancer metabolism --- cancer immunotherapy --- nanoparticles --- immunotherapeutic agent --- immunomodulators --- tuft cells --- cancer stem cells --- immunotherapies --- myeloid-derived suppressor cells --- regulatory T cells --- crosstalk --- tumor immune evasion --- cell-cell contact --- β2 integrins --- CD18 --- CD11 --- CAR-T cells --- CD37 --- cell therapy --- tumor antigen --- lymphoma --- CAR macrophage --- CAR T cell --- solid tumors --- immunometabolism --- miRNA --- immunogenic cell death --- Autophagy --- colorectal cancer --- immunotherapy --- tumor stroma --- tumor microenvironment --- immune checkpoint inhibitors --- chemotherapy --- tyrosine kinase inhibitors --- angiogenesis --- check point inhibitors --- programmed cell death protein 1 --- programmed cell death 1 ligand 1 --- cardiotoxicity --- lung metastasis --- CAR-T --- hypoxia --- tumor --- microenvironment --- CD19 --- BCMA --- cancer --- melanoma --- immune escape --- antigen loss --- chimeric antigen receptor --- electroporation --- lentivirus --- lentiviral transduction --- macrophages --- leukemia cells --- lytic peptides --- targeted therapy --- dendritic cells --- pathogenesis --- risk factors --- breast cancer --- resistance --- checkpoint --- targeted treatment --- personalized medicine --- pediatric solid tumors --- chimeric antigen receptors --- cancer vaccines --- oncolytic viral therapy --- immunomodulation --- DCLK1 --- tumor stem cells --- clonogenicity --- mitochondria --- mitochondrial transfer --- tunneling nanotubes --- triple-negative breast cancer --- immune checkpoint inhibitor --- combination therapy --- cancer nanomedicine --- tumor antigens --- cancer metabolism --- cancer immunotherapy --- nanoparticles --- immunotherapeutic agent --- immunomodulators --- tuft cells --- cancer stem cells --- immunotherapies --- myeloid-derived suppressor cells --- regulatory T cells --- crosstalk --- tumor immune evasion --- cell-cell contact --- β2 integrins --- CD18 --- CD11 --- CAR-T cells --- CD37 --- cell therapy --- tumor antigen --- lymphoma --- CAR macrophage --- CAR T cell --- solid tumors --- immunometabolism --- miRNA --- immunogenic cell death
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