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

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dc.contributor.authorSmith, W.
dc.contributor.authorGuida, L.
dc.contributor.authorQiuy, S.
dc.contributor.authorKorpelainen, E.
dc.contributor.authorvan den Hueven, C.
dc.contributor.authorGillis, D.
dc.contributor.authorHawrylowicz, C.
dc.contributor.authorVadas, M.
dc.contributor.authorLopez, A.
dc.date.issued1995
dc.description.abstractFreshly 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.
dc.description.statementofresponsibilityWB Smith, L Guida, Q Sun, EI Korpelainen, C van den Heuvel, D Gillis, CM Hawrylowicz, MA Vadas, and AF Lopez
dc.identifier.citationBlood, 1995; 86(10):3938-3944
dc.identifier.doi10.1182/blood.v86.10.3938.bloodjournal86103938
dc.identifier.issn0006-4971
dc.identifier.issn1528-0020
dc.identifier.orcidSmith, W. [0000-0001-9640-1172] [0000-0002-4610-998X]
dc.identifier.orcidLopez, A. [0000-0001-7430-0135]
dc.identifier.urihttp://hdl.handle.net/2440/11539
dc.language.isoen
dc.publisherAmerican Society of Hematology
dc.rights© 1995 by The American Society of Hematology
dc.source.urihttp://www.bloodjournal.org/content/86/10/3938
dc.subjectNeutrophils
dc.subjectCells, Cultured
dc.subjectHumans
dc.subjectGranulocyte-Macrophage Colony-Stimulating Factor
dc.subjectInterleukin-3
dc.subjectReceptors, Granulocyte-Macrophage Colony-Stimulating Factor
dc.subjectReceptors, Interleukin-3
dc.subjectRecombinant Proteins
dc.subjectRNA, Messenger
dc.subjectHLA-D Antigens
dc.subjectFlow Cytometry
dc.subjectSignal Transduction
dc.subjectNeutrophil Activation
dc.subjectGene Expression Regulation
dc.titleNeutrophils activated by granulocyte-macrophage colony-stimulating factor express receptors for interleukin-3 which mediate class II expression
dc.typeJournal article
pubs.publication-statusPublished

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