Impaired Production and Increased Apoptosis of Neutrophils in Granulocyte Colony-Stimulating Factor Receptor–Deficient Mice

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...

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Bibliographic Details
Published in:Immunity (Cambridge, Mass.) Mass.), 1996-11, Vol.5 (5), p.491-501
Main Authors: Liu, Fulu, Wu, Huai Yang, Wesselschmidt, Robin, Kornaga, Tad, Link, Daniel C
Format: Article
Language:English
Subjects:
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
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Summary: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.
ISSN:1074-7613
1097-4180
DOI:10.1016/S1074-7613(00)80504-X