Impaired production and increased apoptosis of neutrophils in granulocyte colony-stimulating factor receptor-deficient mice

Immunity. 1996 Nov;5(5):491-501. doi: 10.1016/s1074-7613(00)80504-x.

Abstract

We have generated mice carrying a homozygous null mutation in the granulocyte colony-stimulating factor receptor (G-CSFR) gene. G-CSFR-deficient mice have decreased numbers of phenotypically normal circulating neutrophils. Hematopoietic progenitors are decreased in the bone marrow, and the expansion and terminal differentiation of these progenitors into granulocytes is impaired. Neutrophils isolated from G-CSFR-deficient mice have an increased susceptibility to apoptosis, suggesting that the G-CSFR may also regulate neutrophil survival. These data confirm a role for the G-CSFR as a major regulator of granulopoiesis in vivo and provide evidence that the G-CSFR may regulate granulopoiesis by several mechanisms. However, the data also suggest that G-CSFR-independent mechanisms of granulopoiesis must exist.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / immunology*
  • Cell Division / immunology
  • Hematopoiesis / immunology
  • Hematopoietic Stem Cells / immunology
  • Hematopoietic Stem Cells / pathology
  • Mice
  • Mice, Mutant Strains
  • Mutagenesis, Site-Directed / immunology
  • Neutrophils / immunology
  • Neutrophils / metabolism*
  • Receptors, Granulocyte Colony-Stimulating Factor / deficiency*
  • Receptors, Granulocyte Colony-Stimulating Factor / genetics*

Substances

  • Receptors, Granulocyte Colony-Stimulating Factor