Eosinophils normally comprise less than 5% of the circulating nucleated cells in the peripheral blood. During normal hematopoiesis, eosinophils, like other hematopoietic cells, are derived from hematopoietic stem cells, but the identity of the precursor cell from which eosinophils are derived remains incompletely defined. While there are data supporting the presence of a hybrid precursor with combined characteristics of basophils and eosinophils (1,2), recent evidence suggests that eosinophil development diverges from that of other granulocytes at the granulocyte/monocyte progenitor stage, to yield a phenotypically distinct eosinophil progenitor cell population (3). Recent evidence also reveals cooperation between the transcription factors GATA-1, c/EBP, and PU.1 (particularly GATA-1) to provide important instructive signals for eosinophil formation in vivo (4). For instance, GATA-1-deficient mice fail to develop eosinophil progenitors in fetal liver (5), and targeted disruption of a high-affinity GATA binding site in the GATA-1 promoter leads to selective loss of eosinophil development in vivo (6).
|Original language||English (US)|
|Title of host publication||Myeloproliferative Disorders|
|Subtitle of host publication||Biology and Management|
|Number of pages||26|
|State||Published - Jan 1 2007|
ASJC Scopus subject areas