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The regulation of angiogenesis by tissue cell-macrophage interactions

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889193172 Year: Pages: 113 DOI: 10.3389/978-2-88919-317-2 Language: English
Publisher: Frontiers Media SA
Subject: Physiology --- Science (General)
Added to DOAB on : 2016-02-05 17:24:33
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Angiogenesis is the physiological process where new blood vessels grow from existing ones, in order to replenish tissues suffering from inadequate blood supply. Perhaps the most studied angiogenic process occurs in solid tumors whose growing mass and expanding cells create a constant demand for additional supply of oxygen and nutrients for survival. However, other physiological and clinical conditions, such as wound healing, ischemic events, autoimmune and age-related diseases also involve angiogenesis. Angiogenesis is a well-structured process that begins when oxygen and nutrients are depleted, leading to the release of chemokines and growth factors that attract immune cells, particularly macrophages and endothelial cells to the site. Macrophages that are recruited to the site, as well as tissue cells and endothelial cells, secrete pro-angiogenic mediators that affect endothelial cells and promote angiogenesis. These mediators include growth factors such as vascular endothelial cell growth factor (VEGF), matrix metalloproteinases (MMPs), as well as low levels of mediators that are usually seen as pro-inflammatory but are pro-angiogenic when secreted in low levels (e.g. nitric oxide (NO) and TNFa). Thus, macrophages play a major role in angiogenesis. Macrophages exhibit high plasticity and are capable of shifting between different activation modes and functions according to their changing microenvironment. Small differences in the composition of activating factors (e.g. TLR ligands such as LPS, anti-inflammatory cytokines, ECM molecules) in the microenvironment may differently activate macrophages to yield classically activated macrophages (or M1 macrophages) that can kill pathogen and tumor cells, alternatively activated macrophages (or M2 macrophages) that secrete antiinflammatory cytokines, resolution macrophages (rM?) that are involved in the resolution of inflammation, or regulatory macrophages (e.g. Myeloid-Derived Suppressor Cells - MDSCs) that control the function of other immune cells. In fact, macrophages may be activated in a spectrum of subsets that may differently contribute to angiogenesis, and in particular non-classically activated macrophages such as tumor-associated macrophages (TAMs) and Tie2-expressing monocytes (TEMs) can secrete high amounts of pro-angiogenic factors (e.g. VEGF, MMPs) or low levels of pro-inflammatory mediators (e.g. NO or TNFa) resulting in pro-angiogenic effects. Although the importance of macrophages as major contributors and regulators of the angiogenic process is well documented, less is known about the interactions between macrophages and other cell types (e.g. tumor cells, normal epithelial cells, endothelial cells) that regulate angiogenesis. We still have only limited understanding which proteins or complexes mediate these interactions and whether they require cell-cell contact (e.g. through integrins) or soluble factors (e.g. the EGF-CSF-1 loop), which signaling pathways are triggered in each of the two corresponding cell types, and how this leads to secretion of pro- or antiangiogenic factors in the microenvironment. The regulation of such interactions and through them of angiogenesis, whether through post-translational modifications of proteins or via the involvement of microRNA, is still unclear. The goal of this Research Topic is to highlight these interactions and their regulation in the context of both physiological and pathological conditions.

Cytokines as Players of Neuronal Plasticity and Sensitivity to Environment in Healthy and Pathological Brain

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889197682 Year: Pages: 158 DOI: 10.3389/978-2-88919-768-2 Language: English
Publisher: Frontiers Media SA
Subject: Neurology --- Science (General)
Added to DOAB on : 2016-04-07 11:22:02
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It is now accepted that immune molecules are not only present within the brain during pathology but they exert physiological functions in the "healthy" brain as well. Increasing evidence points to a neuro-modulatory role of cytokines and chemokines (CHEMOtactic cytoKINES) in basal transmission and plasticity processes where signaling between peri-synaptic astrocytes, microglia and neurons plays an important role. Nevertheless, the exact mechanisms as to how cytokines, and in particular chemokines, participate in the molecular and cellular processes thought to subserve memory formation, plasticity processes and responsiveness to environmental stimuli remain to be clarified. Interestingly, in in vitro preparations, molecules like TNF-a, interleukin (IL)-1ß, IL-6, CX3CL1, CXCL12, CCL2 and CCL3 are implicated in synaptic formation and scaling, in modulation of glutamatergic transmission, in plasticity and neurogenesis, in particular in the hippocampus. The hippocampus is an extremely plastic structure, one of the main neurogenic niches in the adult brain, that exhibits a marked sensibility to environmental stimuli. Indeed exposure of mice to environmental enrichment (EE) modifies learning and memory abilities increasing neurogenesis and neuronal plasticity whether exposure to severe stressful experiences diminishes neurotrophic support, impairs neurogenesis, plasticity and cognition. In the hippocampus cytokines play a key role in mediating both positive as well as negative effects of the environment affecting neuronal plasticity also in stress related pathologies, such as depression. It has been reported that mice lacking type 1 receptor for IL-1 display impaired hippocampal memory and LTP that are restored by EE; moreover negative effects on neuronal plasticity (and thus behavior) induced by stress exposure can be prevented by blocking IL-1 activity. In addition, mice lacking IL-6 have improved cognitive functions whereas the absence of microglia-driven CX3CR1 signaling increases hippocampal plasticity and spatial memory occluding the potentiating effects of EE. However, the factors mediating the effect of environmental stimuli on behavior and plasticity has been only partially identified. Interestingly, it has been suggested that chemokines can play a key role in the flexibility of hippocampal structure and may modulate neuronal signaling during behavior. The question is how cytokines may translate environmental stimuli in plasticity and behavioral changes. This research topic is proposed to explore the role of cytokines, and more in particular chemokines, in the modulation of neuronal activity as a fundamental step for the correct brain wiring, function and susceptibility to environment. We encourage the submission of original research reports, review articles, commentaries, perspectives or short communications, in the following (but not limited to) topics:- Role of cytokines and chemokines in neuronal plasticity- Immune molecules and responsiveness to environment- Role of chemokine in the flexibility of hippocampal structure

Chemokines and chemokine receptors in brain homeostasis

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889196166 Year: Pages: 124 DOI: 10.3389/978-2-88919-616-6 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Neurology
Added to DOAB on : 2016-08-16 10:34:25
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Virtually involved in all pathologies that present an inflammatory component, it is now evident that, in the central nervous system, chemokines and chemokine receptors possess pleiotropic properties beyond chemotaxis: costitutive brain expression of chemokines and their receptors on endothelial cells, but also on neurons and glia, suggests a role for such molecules in mediating homeostatic cross-talk between cells of the brain perenchyma. Cross-talk between neurons and glia is determinant to the establishment and maintenance of a brain enviroment that ensure normal function, and in particular glial cells are active players that respond to enviromental changes and act for the survival, growth, differentiation and repair of the nervous tissue: in this regard brain endogenous chemokines represent key molecules that play a role in brain development, neurogenesis, neurotransmission and neuroprotection. As important regulators of peripheral immune response, chemokines are molecules of the immune system that play a central role in coordinating communication between the nervous and the immune systems, in the context of infections and brain injury. Indeed, in phatological processes resulting from infections, brain trauma, ischemia and chronic neurodegenerative diseases, chemokines represent important neuroinflammatory mediators that drive leucocytes trafficking into the central nervous system, facilitating an immune response by targeting cells of the innate and adaptive immune system. The third edition of the international conference "Chemokines and Chemokine Receptors in the Nervous System", hold in Rome in October 2013, represented an exciting platform to promote discussion among researchers in different disciplines to understand the role of chemokines in brain homoestasis. This Frontiers Research Topic arises from this conference, and wants to be an opportunity to further discuss and highlight the importance of brain chemokines as key molecules that, not only grant the interplay between the immune and the nervous systems, but in addition drive modulatory functions on brain homeoastasis orchestrating neurons, microglia, and astrocytes communication.

Immunomodulatory Effects of Drugs for Treatment of Immune-Related Diseases

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889452880 Year: Pages: 108 DOI: 10.3389/978-2-88945-288-0 Language: English
Publisher: Frontiers Media SA
Subject: Medicine (General) --- Allergy and Immunology
Added to DOAB on : 2018-02-27 16:16:44
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More than 90% of diseases possess immunological abnormalities. Disorders such as inflammation, hypersensitivity, autoimmunity and immunodeficiency are simple examples of how the immune system misinterprets its surroundings and goes awry. Multiple sclerosis, rheumatoid arthritis, systemic lupus erythematosus, inflammatory bowel diseases, among many others are manifestations of immune cells attacking normal tissues. On the other hand, damping the immune system leads to diseases such as cancer, AIDS, and severe combined immunodeficiency. The last ten years witnessed an explosion in developing drugs that target the immune system. Several novel monoclonal antibodies have been approved for treatment of various diseases confirming that personalized medicine approach is robust in combating diseases. Hence, the future holds great promise for using personalized and targeted medicine rather than generalized medications that, in most circumstances, proven to be ineffective and characteristically exert side effects. Approaches such as generating novel adjuvants that can stimulate the immune system without harmful side effects, targeting inflammatory cytokines and chemokines, harnessing and activating innate immune cells such as natural killer cells or dendritic cells, are examples of future approaches to treat autoimmune diseases, AIDS, and various forms of cancer resulting from chronic inflammation. More recently, targeting immune checkpoint molecules have shown therapeutic response against lung cancer and melanoma. Identifying molecules involved in autophagy is another example of how personalized medicine might help treat patients with refractory asthma and autoimmune diseases. This topic introduces the reader to these novel approaches of manipulating the immune system and developing targeted therapeutic strategies for treatment of various diseases.

The Role of Aire, microRNAs and Cell-Cell Interactions on Thymic Architecture and Induction of Tolerance

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889197705 Year: Pages: 107 DOI: 10.3389/978-2-88919-770-5 Language: English
Publisher: Frontiers Media SA
Subject: Allergy and Immunology --- Medicine (General)
Added to DOAB on : 2016-04-07 11:22:02
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The focus of this eBook is to bring new insights into central immune tolerance. To fulfill that, much has been discussed about the master in the regulation of tolerance, the autoimmune regulator (Aire) gene the main thymus cell type that expresses this gene, the medullary thymic epithelial cells (mTECs). It includes one Editorial and 12 other excellent contributions in the format of mini reviews or original research papers covering one or more of these aspects: promiscuous gene expression (PGE), epigenetics, miRNAs, association of the Aire gene and miRNAs, thymocyte–TEC interaction, coxsackievirus and type 1 diabetes, exosomes in the thymus, thymic crosstalk, thymic B cells, T cell development, chemokines and migration of T cells, miRNAs and the thymic atrophy, cell–cell interactions, and thymus ontogeny. Authors raised hypothesis, discuss concepts, and show open questions. The remaining important issues to resolve questions within the central tolerance research are briefly discussed below.

Research of Pathogenesis and Novel Therapeutics in Arthritis

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ISBN: 9783038970651 / 9783038970668 Year: Pages: 366 DOI: 10.3390/books978-3-03897-066-8 Language: eng
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Medicine (General) --- Therapeutics
Added to DOAB on : 2019-06-26 08:44:06
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Arthritis has a high prevalence globally and includes over 100 different types, the most common of which are rheumatoid arthritis, osteoarthritis, psoriatic arthritis, and inflammatory arthritis. The exact etiology of arthritis remains unclear and no cure exists. Anti-inflammatory drugs are commonly used in the treatment of arthritis but are associated with significant side effects. Novel modes of therapy and additional prognostic biomarkers are urgently needed for arthritis patients. This book summarizes and discusses the global picture of the current understanding of arthritis.

Keywords

biosimilars --- Th9 lymphocytes --- rheumatoid arthritis --- infliximab --- rheumatoid arthritis --- bone erosion --- osteoblasts --- next-generation sequencing --- bioinformatics --- microRNA --- messenger RNA --- osteoarthritis --- cell signaling --- IL1? --- WNT --- antagonists --- computational modeling --- nitric oxide --- clodronate --- gene expression --- osteoarthritis --- progenitor cells --- SOX9 --- spondyloarthropathies --- inflammation --- mesenchymal stem cells --- visfatin --- IL-6 --- TNF-? --- osteoarthritis --- miR-199a-5p --- Epstein-Barr virus --- glycoprotein 42 --- rheumatoid arthritis --- shared epitope --- triptolide --- rheumatoid arthritis --- basic research --- clinical translation --- osteoarthritis (OA) --- articular cartilage --- molecular pathology --- therapeutics --- rheumatoid arthritis --- antibodies --- collagen --- glycosylation --- disease pathways --- therapy --- experimental arthritis --- TNF? --- etanercept --- infliximab --- adalimumab --- certolizumab pegol --- golimumab --- rheumatoid arthritis --- therapeutic antibody --- structure --- fraxinellone --- collagen-induced arthritis --- rheumatoid arthritis --- inflammatory arthritis --- osteoclastogenesis --- sclareol --- rheumatoid arthritis --- synovial cell --- collagen --- mice --- cytokines --- Th17 --- MAPK --- arthritis --- osteoarthritis --- rheumatoid arthritis --- small-molecule inhibitor --- chondrocytes --- tumor necrosis factor-alpha --- inflammation --- rheumatoid arthritis --- osteoarthritis --- angiogenesis --- cytokines --- chemokines --- early osteoarthritis --- articular cartilage --- proliferation --- fibroblast growth factor 2 --- mitogen activated protein kinase --- transforming growth factor ? --- SMA- and MAD-related protein --- interleukin --- nuclear factor kappa B --- miRNA --- adjuvant arthritis --- arthritis --- biomarkers --- celastrol --- inflammation --- microRNA --- miRNA --- rat --- rheumatoid arthritis --- Traditional Chinese medicine --- tripterine --- triterpenoid --- spinal fusion --- biological --- osteoblast --- osteoclast --- bisphosphonate --- parathyroid hormone --- bone morphogenetic protein --- receptor activator of nuclear factor ?B --- stem cell --- drug delivery system --- anticitrullinated peptide antibodies --- antirheumatic drug --- autoimmune --- disease-modifying --- immunology --- pathology --- rheumatoid factor --- rheumatoid arthritis --- osteoarthritis --- adipokines --- obesity --- rheumatoid arthritis --- osteoarthritis --- anti-arthritis --- biomarkers

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