Macrophage Activation and Polarization: Nomenclature and Experimental Guidelines

Immunity, Journal Year: 2014, Volume and Issue: 41(1), P. 14 - 20

Published: July 1, 2014

Language: Английский

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AKT/PKB Signaling: Navigating the Network

Cell, Journal Year: 2017, Volume and Issue: 169(3), P. 381 - 405

Published: April 1, 2017

Language: Английский

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Network Integration of Parallel Metabolic and Transcriptional Data Reveals Metabolic Modules that Regulate Macrophage Polarization

Immunity, Journal Year: 2015, Volume and Issue: 42(3), P. 419 - 430

Published: March 1, 2015

Language: Английский

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The Metabolic Signature of Macrophage Responses

Frontiers in Immunology, Journal Year: 2019, Volume and Issue: 10

Published: July 3, 2019

Macrophages are a heterogeneous population of immune cells playing several and diverse functions in homeostatic responses. The broad spectrum macrophage depends on both heterogeneity plasticity these cells, which highly specialized sensing the microenvironment modify their properties accordingly. Although it is clear that phenotypes difficult to categorize should be seen as plastic adaptable, they can simplified into two extremes: pro-inflammatory (M1) an anti-inflammatory/pro-resolving (M2) profile. Based this definition, M1 macrophages able start sustain inflammatory responses, secreting cytokines, activating endothelial inducing recruitment other inflamed tissue; hand, M2 promote resolution inflammation, phagocytose apoptotic drive collagen deposition, coordinate tissue integrity, release anti-inflammatory mediators. Dramatic switches cell metabolism accompany phenotypic functional changes macrophages. In particular, rely mainly glycolysis present breaks TCA cycle result accumulation itaconate (a microbicide compound) succinate. Excess succinate leads Hypoxia Inducible Factor 1 (HIF1) stabilization that, turn, activates transcription glycolytic genes, thus sustaining On contrary, more dependent oxidative phosphorylation (OXPHOS), intact provides substrates for complexes electron transport chain (ETC). Moreover, pro- characterized by specific pathways regulate lipids amino acids affect All metabolic adaptations support activities well polarization contexts. aim review discuss recent findings linking metabolism.

Language: Английский

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Metabolic reprogramming in macrophages and dendritic cells in innate immunity

Cell Research, Journal Year: 2015, Volume and Issue: 25(7), P. 771 - 784

Published: June 5, 2015

Activation of macrophages and dendritic cells (DCs) by pro-inflammatory stimuli causes them to undergo a metabolic switch towards glycolysis away from oxidative phosphorylation (OXPHOS), similar the Warburg effect in tumors. However, it is only recently that mechanisms responsible for this reprogramming have been elucidated more detail. The transcription factor hypoxia-inducible factor-1α (HIF-1α) plays an important role under conditions both hypoxia normoxia. withdrawal citrate tricarboxylic acid (TCA) cycle has shown be critical lipid biosynthesis DCs. Interference with process actually abolishes ability DCs activate T cells. Another TCA intermediate, succinate, activates HIF-1α promotes inflammatory gene expression. These new insights are providing us deeper understanding innate immunity.

Language: Английский

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PI3Kγ is a molecular switch that controls immune suppression

Nature, Journal Year: 2016, Volume and Issue: 539(7629), P. 437 - 442

Published: Sept. 16, 2016

Language: Английский

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Akt Signaling Pathway in Macrophage Activation and M1/M2 Polarization

The Journal of Immunology, Journal Year: 2017, Volume and Issue: 198(3), P. 1006 - 1014

Published: Jan. 23, 2017

Abstract Macrophages become activated initiating innate immune responses. Depending on the signals, macrophages obtain an array of activation phenotypes, described by broad terms M1 or M2 phenotype. The PI3K/Akt/mTOR pathway mediates signals from multiple receptors including insulin receptors, pathogen-associated molecular pattern cytokine adipokine and hormones. As a result, Akt converges inflammatory metabolic to regulate macrophage responses modulating their is family three serine-threonine kinases, Akt1, Akt2, Akt3. Generation mice lacking individual Akt, PI3K, mTOR isoforms utilization RNA interference technology have revealed that signaling components distinct isoform-specific roles in biology disease regulation, controlling cytokines, miRNAs, functions phagocytosis, autophagy, cell metabolism. Herein, we review current knowledge role macrophages, focusing M1/M2 polarization highlighting isoform–specific functions.

Language: Английский

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Regulation of innate immune cell function by mTOR

Nature reviews. Immunology, Journal Year: 2015, Volume and Issue: 15(10), P. 599 - 614

Published: Sept. 25, 2015

Language: Английский

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Metabolic Reprogramming of Immune Cells in Cancer Progression

Immunity, Journal Year: 2015, Volume and Issue: 43(3), P. 435 - 449

Published: Sept. 1, 2015

Language: Английский

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Macrophage phenotypes in atherosclerosis

Immunological Reviews, Journal Year: 2014, Volume and Issue: 262(1), P. 153 - 166

Published: Oct. 15, 2014

Summary Initiation and progression of atherosclerosis depend on local inflammation accumulation lipids in the vascular wall. Although many cells are involved development atherosclerosis, macrophages fundamental contributors. For nearly a decade, phenotypic heterogeneity plasticity has been studied. In atherosclerotic lesions, submitted to large variety micro‐environmental signals, such as oxidized cytokines, which influence polarization activation resulting dynamic plasticity. The macrophage phenotype spectrum is characterized, at extremes, by classical M1 induced T‐helper 1 (Th‐1) cytokines alternative M2 Th‐2 cytokines. can be further classified into M2a, M2b, M2c, M2d subtypes. More recently, additional plaque‐specific phenotypes have identified, termed Mox, Mhem, M4. Understanding mechanisms functional consequences will contribute determine their potential role lesion plaque stability. Furthermore, research could lead novel therapeutic approaches counteract cardiovascular diseases atherosclerosis. present review summarizes our current knowledge subsets plaques mechanism behind modulation phenotype.

Language: Английский

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