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Resolution of inflammation: an integrated view

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TLDR
This review integrates the key molecular and cellular mechanisms of resolution and describes how abrogation of chemokine signalling blocks continued neutrophil tissue infiltration and how apoptotic neutrophils attract monocytes and macrophages to induce their clearance.
Abstract
Resolution of inflammation is a coordinated and active process aimed at restoration of tissue integrity and function. This review integrates the key molecular and cellular mechanisms of resolution. We describe how abrogation of chemokine signalling blocks continued neutrophil tissue infiltration and how apoptotic neutrophils attract monocytes and macrophages to induce their clearance. Uptake of apoptotic neutrophils by macrophages reprograms macrophages towards a resolving phenotype, a key event to restore tissue homeostasis. Finally, we highlight the therapeutic potential that derives from understanding the mechanisms of resolution.

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Microglial M1/M2 polarization and metabolic states.

TL;DR: The polarization states of microglia and their relationship to mitochondrial metabolism are examined and a role of metabolic reprogramming in the regulation of the innate inflammatory response is suggested.
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Inflammation, fracture and bone repair

TL;DR: In this review, a comprehensive summary of the literature related to inflammation and bone repair is provided, placing special emphasis on the underlying cellular and molecular mechanisms, and potential interventions that can favorably modulate the outcome of clinical conditions that involve bone repair.
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Inflammation following acute myocardial infarction: Multiple players, dynamic roles, and novel therapeutic opportunities.

TL;DR: An overview of the multiple players (and their dynamic roles) involved in the complex inflammatory response to AMI and subsequent LV remodeling is provided, and future opportunities for targeting inflammation as a therapeutic strategy for limiting MI size, preventing adverse left ventricular remodeling, and reducing heart failure in AMI patients are highlighted.
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Neutrophils orchestrate post-myocardial infarction healing by polarizing macrophages towards a reparative phenotype

TL;DR: Neutrophils are crucially involved in cardiac repair after MI by polarizing macrophages towards a reparative phenotype, andTherapeutic strategies to reduce acute neutrophil-driven inflammation after MI should be carefully balanced as they might interfere with the healing response and cardiac remodelling.
References
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Journal ArticleDOI

Control of Regulatory T Cell Development by the Transcription Factor Foxp3

TL;DR: Foxp3, which encodes a transcription factor that is genetically defective in an autoimmune and inflammatory syndrome in humans and mice, is specifically expressed in naturally arising CD4+ regulatory T cells and retroviral gene transfer of Foxp3 converts naïve T cells toward a regulatory T cell phenotype similar to that of naturally occurring CD4+.
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Myeloid-derived suppressor cells as regulators of the immune system.

TL;DR: The origin, mechanisms of expansion and suppressive functions of MDSCs, as well as the potential to target these cells for therapeutic benefit are discussed.
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Mesenchymal stem cells in health and disease

TL;DR: The targets and mechanisms of M SC-mediated immunomodulation and the possible translation of MSCs to new therapeutic approaches are discussed.
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Macrophages that have ingested apoptotic cells in vitro inhibit proinflammatory cytokine production through autocrine/paracrine mechanisms involving TGF-beta, PGE2, and PAF.

TL;DR: The results suggest that binding and/or phagocytosis of apoptotic cells induces active antiinflammatory or suppressive properties in human macrophages, likely that resolution of inflammation depends not only on the removal of apoptosis but on active suppression of inflammatory mediator production.
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