title: Neutrophil apoptosis and its induction as a potential treatment for chronic inflammatory disease.
abstract: OBJECTIVE
  Neutrophils are a key component of innate immunity. At sites of infection, they unleash cytotoxic molecules allowing them to kill invading pathogens. However, these molecules can also be deleterious to the host tissue. Therefore, neutrophils undergo apoptosis and are removed from the site of infection following elimination of the pathogen. When neutrophil apoptosis is significantly delayed, this can result in chronic inflammation. This review highlights recent advances in our understanding of neutrophil apoptosis, and discusses literature surrounding the induction of neutrophil apoptosis as a therapeutic strategy for the treatment of chronic inflammatory disease.
  
  
  RESULTS
  Recent studies have highlighted the role of cyclin-dependent kinases (CDKs) in the regulation of neutrophil lifespan. CDK activity appears to be involved in the maintenance of levels of Mcl-1, an antiapoptotic Bcl-2 family member. In addition, recent findings have demonstrated the induction of neutrophil apoptosis at sites of infection by bystander immune cells including T-regulatory cells (Tregs) and natural killer (NK) cells.
  
  
  CONCLUSIONS
  Recent advances in our understanding of the processes involved in neutrophil apoptosis, coupled with new insights into the mechanisms by which bystander immune cells induce neutrophil death, may provide novel and exciting possibilities with regards to the treatment of chronic inflammatory diseases.
authors.affiliation: MRC-ARUK Centre for Musculoskeletal Ageing Research, Centre for Translational Inflammation Research, School of Immunity and Infection, University of Birmingham, Birmingham, UK. p.hampson@bham.ac.uk
authors.forename: Peter
authors.initials: P
authors.lastname: Hampson
authors.forename: Jon
authors.initials: J
authors.lastname: Hazeldine
authors.forename: Janet M
authors.initials: JM
authors.lastname: Lord
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000276:immunology*; D002908:Chronic Disease; D006801:Humans; D007249:Inflammation / Q000276:immunology* / Q000628:therapy*; D009504:Neutrophils / Q000166:cytology / Q000276:immunology* / Q000473:pathology