Abstract
G-CSF is produced by a variety of cells. In situ hybridization showed that only a small proportion of stromal cells expressed G-CSF after stimulation with LPS or IL-1. The measurement of serum G-CSF level by enzyme immunoassay provided valuable information as to the pathophysiological roles of G-CSF. In aplastic anemia, there was an inverse correlation between blood neutrophil count and serum G-CSF level. Similarly, the G-CSF level rose during the neutropenic phase of cyclic neutropenia. These findings suggest that the serum G-CSF level is regulated by a feedback mechanism. In some cases, the reduced G-CSF production by stromal cells may underlie the pathogenesis of neutropenia. On the other hand, infections and cancers sometimes caused high serum G-CSF levels in association with increased blood neutrophils, presumably reflecting reactive and aberrant production of G-CSF, respectively. Expression of G-CSF by myeloid leukemia cells may partly contribute to their abnormal growth through the autocrine mechanism.
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