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Apoptosis in resolution of inflammation

Journal of Leukocyte Biology · 1997 · Vol. 61(4) · pp. 375–380
John Savill

Abstract

The last few years have seen the accumulation of compelling evidence that apoptosis (programmed cell death) plays a major role in promoting resolution of the acute inflammatory response. Neutrophils are constitutively programmed to undergo apoptosis, which limits their pro-inflammatory potential and leads to rapid, specific, and non-phlogistic recognition by macrophages and semi-professional phagocytes. Similar mechanisms have been implicated in clearance of eosinophils, lymphocytes, and monocytes and apoptosis also plays a role in remodeling the inflamed site by deletion of myofibroblasts. A growing understanding of the mechanisms regulating leukocyte apoptosis and of the molecules mediating safe phagocytic clearance of dying cells may yield new insights into the pathogenesis and therapy of inflammatory diseases.

Neutrophil, Myeloperoxidase and Oxidative MechanismsImmune Response and InflammationInflammasome and immune disordersApoptosisInflammationBiologyProgrammed cell deathCell biologyPathogenesisMacrophageImmunologyEfferocytosisCancer research

MeSH terms

AnimalsGranulocytesHumansInflammationMacrophagesNeutrophilsPhagocytosisApoptosis

Funding

  • Wellcome Trust
  • Society for Leukocyte Biology
  • Medical Research Council
Citations
653
FWCI
11.33
field-weighted impact
References
52
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99%
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