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

Immunity (1996-11-01)
F Liu, H Y Wu, R Wesselschmidt, T Kornaga, D C Link
RESUMEN

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.

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Sigma-Aldrich
Anti-Granulocyte Colony Stimulating Factor antibody produced in goat, IgG fraction of antiserum, lyophilized powder
Sigma-Aldrich
Anti-Granulocyte Colony Stimulating Factor antibody produced in goat, IgG fraction of antiserum, lyophilized powder
Sigma-Aldrich
Monoclonal Anti-Granulocyte Colony Stimulating Factor antibody produced in rat, clone 67604, purified immunoglobulin, lyophilized powder

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