title: Reduced expression of hemopoietic cytokine receptors on cord blood progenitor cells in neonates at risk for atopy.
abstract: BACKGROUND
  Recent findings point to an association between allergic asthma in adults and increased responsiveness of myeloid progenitor cells to certain hemopoietic growth factors. However, it is not clear at what age these changes in progenitor cells first become manifest, although increasing evidence suggests that the allergic phenotype may begin to emerge in very early life.
  
  
  OBJECTIVE
  We sought to compare expression of hemopoietic cytokine receptors on CD34(+) progenitor cells in cord blood from normal infants ("low risk" for subsequent atopy) and infants with at least one atopic first degree relative ("at risk" for subsequent atopy).
  
  
  METHODS
  Cord blood was obtained from 21 neonates. Nonadherent mononuclear cells were stained with mAbs directed against CD45, CD34, and the alpha-chains of the GM-CSF, IL-3, and IL-5 receptors and analyzed by flow cytometry.
  
  
  RESULTS
  No differences in absolute CD34(+) numbers were observed between the 2 groups. However, expression of GM-CSF receptor on CD34(+) cells was reduced in the "at-risk" compared with the "low- risk" group (P =.021), although no significant differences were noted between the 2 groups with respect to IL-3 and IL-5 receptor expression.
  
  
  CONCLUSIONS
  The functional sequelae of reduced GM-CSF receptor expression on CD34(+) cells remain to be determined. Nonetheless, these findings show an association between genetic risk for atopy and changes in the expression of hemopoietic cytokine receptors on cord blood progenitor cells and support the notion that the allergic phenotype may begin to evolve in the perinatal period.
authors.affiliation: Division of Clinical Immunology and Allergy, Department of Medicine, McMaster University, Hamilton, Ontario, Canada.
authors.forename: J W
authors.initials: JW
authors.lastname: Upham
authors.forename: L M
authors.initials: LM
authors.lastname: Hayes
authors.forename: J
authors.initials: J
authors.lastname: Lundahl
authors.forename: R
authors.initials: R
authors.lastname: Sehmi
authors.forename: J A
authors.initials: JA
authors.lastname: Denburg
mesh_terms: D000328:Adult; D018952:Antigens, CD34 / Q000097:blood; D017252:CD3 Complex / Q000097:blood; D005260:Female; D005312:Fetal Blood / Q000166:cytology* / Q000276:immunology; D020022:Genetic Predisposition to Disease / Q000453:epidemiology; D006412:Hematopoietic Stem Cells / Q000737:chemistry* / Q000276:immunology / Q000378:metabolism; D006801:Humans; D006969:Hypersensitivity, Immediate / Q000097:blood* / Q000453:epidemiology / Q000235:genetics; D007231:Infant, Newborn; D011247:Pregnancy; D018121:Receptors, Cytokine / Q000096:biosynthesis*; D016187:Receptors, Granulocyte-Macrophage Colony-Stimulating Factor / Q000096:biosynthesis; D017978:Receptors, Growth Factor / Q000097:blood; D017452:Receptors, IgG / Q000097:blood; D018123:Receptors, Interleukin / Q000096:biosynthesis; D016185:Receptors, Interleukin-3 / Q000096:biosynthesis; D053649:Receptors, Interleukin-5; D012307:Risk Factors
chemical_list: D018952:Antigens, CD34; D017252:CD3 Complex; D018121:Receptors, Cytokine; D016187:Receptors, Granulocyte-Macrophage Colony-Stimulating Factor; D017978:Receptors, Growth Factor; D017452:Receptors, IgG; D018123:Receptors, Interleukin; D016185:Receptors, Interleukin-3; D053649:Receptors, Interleukin-5