Reactive Oxygen Species in Inflammation and Tissue Injury

Antioxidants and Redox Signaling, Journal Year: 2013, Volume and Issue: 20(7), P. 1126 - 1167

Published: Sept. 2, 2013

Abstract Reactive oxygen species (ROS) are key signaling molecules that play an important role in the progression of inflammatory disorders. An enhanced ROS generation by polymorphonuclear neutrophils (PMNs) at site inflammation causes endothelial dysfunction and tissue injury. The vascular endothelium plays passage macromolecules cells from blood to tissue. Under conditions, oxidative stress produced PMNs leads opening inter-endothelial junctions promotes migration across barrier. migrated not only help clearance pathogens foreign particles but also lead current review compiles past research area with particular emphasis on stress-mediated mechanisms involved

Language: Английский

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Chemokines and Chemokine Receptors: Positioning Cells for Host Defense and Immunity

Annual Review of Immunology, Journal Year: 2014, Volume and Issue: 32(1), P. 659 - 702

Published: March 21, 2014

Chemokines are chemotactic cytokines that control the migratory patterns and positioning of all immune cells. Although chemokines were initially appreciated as important mediators acute inflammation, we now know this complex system approximately 50 endogenous chemokine ligands 20 G protein–coupled seven-transmembrane signaling receptors is also critical for generation primary secondary adaptive cellular humoral responses. Recent studies demonstrate roles in priming naive T cells, cell fate decisions such effector memory differentiation, regulatory function. In review, focus on recent advances understanding how orchestrates migration at organismic level homeostasis, during regulation adoptive responses lymphoid peripheral nonlymphoid tissue.

Language: Английский

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Roles of the immune system in cancer: from tumor initiation to metastatic progression

Genes & Development, Journal Year: 2018, Volume and Issue: 32(19-20), P. 1267 - 1284

Published: Oct. 1, 2018

The presence of inflammatory immune cells in human tumors raises a fundamental question oncology: How do cancer avoid the destruction by attack? In principle, tumor development can be controlled cytotoxic innate and adaptive cells; however, as develops from neoplastic tissue to clinically detectable tumors, evolve different mechanisms that mimic peripheral tolerance order tumoricidal attack. Here, we provide an update recent accomplishments, unifying concepts, future challenges study tumor-associated cells, with emphasis on metastatic carcinomas.

Language: Английский

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The Biological Basis for Cardiac Repair After Myocardial Infarction

Circulation Research, Journal Year: 2016, Volume and Issue: 119(1), P. 91 - 112

Published: June 24, 2016

In adult mammals, massive sudden loss of cardiomyocytes after infarction overwhelms the limited regenerative capacity myocardium, resulting in formation a collagen-based scar. Necrotic cells release danger signals, activating innate immune pathways and triggering an intense inflammatory response. Stimulation toll-like receptor signaling complement activation induces expression proinflammatory cytokines (such as interleukin-1 tumor necrosis factor-α) chemokines monocyte chemoattractant protein-1/ chemokine (C-C motif) ligand 2 [CCL2]). Inflammatory signals promote adhesive interactions between leukocytes endothelial cells, leading to extravasation neutrophils monocytes. As infiltrating clear infarct from dead mediators repressing inflammation are released, anti-inflammatory mononuclear cell subsets predominate. Suppression response is associated with reparative cells. Fibroblasts proliferate, undergo myofibroblast transdifferentiation, deposit large amounts extracellular matrix proteins maintaining structural integrity infarcted ventricle. The renin-angiotensin-aldosterone system members transforming growth factor-β family play important role myofibroblasts. Maturation scar follows, network cross-linked collagenous formed granulation tissue become apoptotic. This review discusses cellular effectors molecular regulating myocardial infarction. Dysregulation pathways, impaired suppression postinfarction inflammation, perturbed spatial containment response, overactive fibrosis may cause adverse remodeling patients contributing pathogenesis heart failure. Therapeutic modulation hold promise for prevention

Language: Английский

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Inflammation and tumor progression: signaling pathways and targeted intervention

Signal Transduction and Targeted Therapy, Journal Year: 2021, Volume and Issue: 6(1)

Published: July 12, 2021

Abstract Cancer development and its response to therapy are regulated by inflammation, which either promotes or suppresses tumor progression, potentially displaying opposing effects on therapeutic outcomes. Chronic inflammation facilitates progression treatment resistance, whereas induction of acute inflammatory reactions often stimulates the maturation dendritic cells (DCs) antigen presentation, leading anti-tumor immune responses. In addition, multiple signaling pathways, such as nuclear factor kappa B (NF-kB), Janus kinase/signal transducers activators transcription (JAK-STAT), toll-like receptor (TLR) cGAS/STING, mitogen-activated protein kinase (MAPK); factors, including cytokines (e.g., interleukin (IL), interferon (IFN), necrosis (TNF)-α), chemokines C-C motif chemokine ligands (CCLs) C-X-C (CXCLs)), growth factors vascular endothelial (VEGF), transforming (TGF)-β), inflammasome; well metabolites prostaglandins, leukotrienes, thromboxane, specialized proresolving mediators (SPM), have been identified pivotal regulators initiation resolution inflammation. Nowadays, local irradiation, recombinant cytokines, neutralizing antibodies, small-molecule inhibitors, DC vaccines, oncolytic viruses, TLR agonists, SPM developed specifically modulate in cancer therapy, with some these already undergoing clinical trials. Herein, we discuss crosstalk between processes. We also highlight potential targets for harnessing cancer.

Language: Английский

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Immune regulation by glucocorticoids

Nature reviews. Immunology, Journal Year: 2017, Volume and Issue: 17(4), P. 233 - 247

Published: Feb. 13, 2017

Language: Английский

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Neutrophil extracellular traps enriched in oxidized mitochondrial DNA are interferogenic and contribute to lupus-like disease

Nature Medicine, Journal Year: 2016, Volume and Issue: 22(2), P. 146 - 153

Published: Jan. 18, 2016

Language: Английский

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Mesenchymal Stromal Cells: Sensors and Switchers of Inflammation

Cell stem cell, Journal Year: 2013, Volume and Issue: 13(4), P. 392 - 402

Published: Oct. 1, 2013

Language: Английский

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The Multifaceted Functions of Neutrophils

Annual Review of Pathology Mechanisms of Disease, Journal Year: 2013, Volume and Issue: 9(1), P. 181 - 218

Published: Sept. 20, 2013

Neutrophils and neutrophil-like cells are the major pathogen-fighting immune in organisms ranging from slime molds to mammals. Central their function is ability be recruited sites of infection, recognize phagocytose microbes, then kill pathogens through a combination cytotoxic mechanisms. These include production reactive oxygen species, release antimicrobial peptides, recently discovered expulsion nuclear contents form neutrophil extracellular traps. Here we discuss these primordial functions, which also play key roles tissue injury, by providing details functions congenital disorders neutrophils. In addition, present more recent evidence that interactions between neutrophils adaptive establish feed-forward mechanism amplifies pathologic inflammation. newly appreciated contributions described setting several inflammatory autoimmune diseases.

Language: Английский

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Immune cells within the tumor microenvironment: Biological functions and roles in cancer immunotherapy

Cancer Letters, Journal Year: 2019, Volume and Issue: 470, P. 126 - 133

Published: Nov. 13, 2019

Language: Английский

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