Neutrophils activated by granulocyte-macrophage colony-stimulating factor express receptors for interleukin-3 which mediate class II expression

Blood. 1995 Nov 15;86(10):3938-44.


Freshly isolated peripheral blood neutrophils, unlike monocytes and eosinophils, do not bind interleukin-3 (IL-3) or respond to IL-3). We show that neutrophils cultured for 24 hours in granulocyte-macrophage colony-stimulating factor (GM-CSF) express mRNA for the IL-3 receptor (R) alpha subunit, as shown by RNase protection assays, and IL-3R alpha chain protein, as shown by cytometric analysis using two different specific monoclonal antibodies. This effect was selective for GM-CSF, because granulocyte colony-stimulating factor, tumor necrosis factor-alpha, interferon-gamma, and IL-1 failed to induce the IL-3 receptor. Saturation binding curves with 125I-IL-3 and Scatchard transformation showed the presence of about 100 high-affinity and 4,000 low-affinity receptors. Because neutrophils have been shown to express human leukocyte antigen (HLA)-DR in response to GM-CSF, we examined the possibility that IL-3 could augment HLA-DR expression on GM-CSF-treated cells. We found that neutrophils incubated with 30 ng/mL IL-3 as well as 0.1 ng/mL GM-CSF expressed a mean of 2.1-fold higher levels of HLA-DR than with GM-CSF alone (P < .005), confirming the signaling competence of the newly expressed IL-3R. This increase was seen even at maximal concentrations of GM-CSF and IL-3 can have an additive effect on mature human cells. The augmentation of HLA-DR by IL-3 was specific because it could be inhibited by a blocking anti-IL-3R antibody. Expression of class II molecules by neutrophils under these conditions may have significance for antigen presentation. These results provide further evidence for the role of GM-CSF as an amplification factor in inflammation by inducing neutrophil responsiveness to IL-3 produced by T cells or mast cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cells, Cultured
  • Flow Cytometry
  • Gene Expression Regulation / drug effects*
  • Granulocyte-Macrophage Colony-Stimulating Factor / pharmacology*
  • HLA-D Antigens / biosynthesis*
  • HLA-D Antigens / genetics
  • Humans
  • Interleukin-3 / metabolism
  • Interleukin-3 / pharmacology*
  • Neutrophil Activation / drug effects*
  • Neutrophils / drug effects*
  • Neutrophils / immunology
  • Neutrophils / metabolism
  • RNA, Messenger / biosynthesis
  • Receptors, Granulocyte-Macrophage Colony-Stimulating Factor / analysis
  • Receptors, Granulocyte-Macrophage Colony-Stimulating Factor / biosynthesis
  • Receptors, Granulocyte-Macrophage Colony-Stimulating Factor / genetics
  • Receptors, Interleukin-3 / analysis
  • Receptors, Interleukin-3 / biosynthesis
  • Receptors, Interleukin-3 / genetics
  • Receptors, Interleukin-3 / physiology*
  • Recombinant Proteins / pharmacology*
  • Signal Transduction


  • HLA-D Antigens
  • Interleukin-3
  • RNA, Messenger
  • Receptors, Granulocyte-Macrophage Colony-Stimulating Factor
  • Receptors, Interleukin-3
  • Recombinant Proteins
  • Granulocyte-Macrophage Colony-Stimulating Factor