IMR Press / FBL / Volume 12 / Issue 3 / DOI: 10.2741/2103

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

Granulocyte colony-stimulating factor and its receptor in normal myeloid cell development, leukemia and related blood cell disorders
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1 Department of Hematology, Erasmus University Medical Center, P.O. Box 1738, 3000 DR, Rotterdam, The Netherlands
Front. Biosci. (Landmark Ed) 2007, 12(3), 800–815;
Published: 1 January 2007

Granulocyte colony-stimulating factor (G-CSF) is the major hematopoietic cytokine involved in the control of neutrophil production and thus serves as a critical regulator of the innate immunity against bacterial infections. G-CSF is applied on a routine basis in the clinic for treatment of congenital and acquired neutropenias, diseases characterized by a critical shortage of neutrophils, leading to severe opportunistic bacterial infections. Very recently, it has become clear that therapeutic application of G-CSF may not be limited to different types of neutropenia, but may extend to non-hematological conditions, in particular cardiac and brain infarctions. G-CSF drives the proliferation, survival and neutrophilic differentiation of myeloid progenitor cells by activation of a receptor of the hematopoietin receptor superfamily, which subsequently triggers multiple signaling mechanisms. These mechanisms exert positive as well as negative effects on the signaling function of the G-CSF receptor. The integrated output of these signaling pathways provide the appropriate balance needed for accurate production of neutrophils under both steady state and "emergency" conditions. Here we review how these mechanisms are thought to act in concert to meet with these demands and how perturbations in the function of the G-CSF receptor are implicated in various types of myeloid disease.

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