Regulation of eosinophil apoptosis: transduction of survival and death signals

Int Arch Allergy Immunol. 1999 Jan;118(1):7-14. doi: 10.1159/000024025.

Abstract

Since eosinophils are prominent in allergic inflammation, investigators became interested in how these cells accumulate in tissues and their role within the inflammatory cascade. There is increasing evidence from several laboratories that eosinophil numbers are regulated in vivo, not only by eosinophil production in the bone marrow, but also by the amount of eosinophil apoptosis. Moreover, it has been directly demonstrated that eosinophil apoptosis is delayed in allergic inflammatory sites, and that this mechanism contributes to the expansion of these cells in tissue. In this article, we review recent studies that shed light on the intracellular pathways that control eosinophil apoptosis.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Animals
  • Apoptosis*
  • Cell Death
  • Cell Survival
  • Eosinophils / physiology*
  • Humans
  • Models, Molecular
  • Nitric Oxide / physiology
  • Receptors, Granulocyte-Macrophage Colony-Stimulating Factor / physiology
  • Receptors, Interleukin / physiology
  • Signal Transduction / physiology*
  • Transforming Growth Factor beta / physiology
  • fas Receptor / physiology

Substances

  • Receptors, Granulocyte-Macrophage Colony-Stimulating Factor
  • Receptors, Interleukin
  • Transforming Growth Factor beta
  • fas Receptor
  • Nitric Oxide