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      Macrophages and the Recovery from Acute and Chronic Inflammation

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          Abstract

          In recent years, researchers have devoted much attention to the diverse roles of macrophages and their contributions to tissue development, wound healing, and angiogenesis. What should not be lost in the discussions regarding the diverse biology of these cells is that when perturbed, macrophages are the primary contributors to potentially pathological inflammatory processes. Macrophages stand poised to rapidly produce large amounts of inflammatory cytokines in response to danger signals. The production of these cytokines can initiate a cascade of inflammatory mediator release that can lead to wholesale tissue destruction. The destructive inflammatory capability of macrophages is amplified by exposure to exogenous interferon-γ, which prolongs and heightens inflammatory responses. In simple terms, macrophages can thus be viewed as incendiary devices with hair triggers waiting to detonate. We have begun to ask questions about how these cells can be regulated to mitigate the collateral destruction associated with macrophage activation.

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          Author and article information

          Journal
          0370600
          674
          Annu Rev Physiol
          Annu. Rev. Physiol.
          Annual review of physiology
          0066-4278
          1545-1585
          13 April 2018
          07 December 2016
          10 February 2017
          23 April 2018
          : 79
          : 567-592
          Affiliations
          Department of Cell Biology and Molecular Genetics, Maryland Pathogen Research Institute, University of Maryland, College Park, Maryland 20742
          Article
          PMC5912892 PMC5912892 5912892 nihpa958418
          10.1146/annurev-physiol-022516-034348
          5912892
          27959619
          b183f949-13a8-46c7-b1ed-9467738f5357
          History
          Categories
          Article

          TLR,cytokines,transcription,prostaglandin,adenosine,NF-κB
          TLR, cytokines, transcription, prostaglandin, adenosine, NF-κB

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