PMID- 7579364
OWN - NLM
STAT- MEDLINE
DCOM- 19951219
LR  - 20210216
IS  - 0006-4971 (Print)
IS  - 0006-4971 (Linking)
VI  - 86
IP  - 10
DP  - 1995 Nov 15
TI  - Neutrophils activated by granulocyte-macrophage colony-stimulating factor express 
      receptors for interleukin-3 which mediate class II expression.
PG  - 3938-44
AB  - 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.
FAU - Smith, W B
AU  - Smith WB
AD  - Department of Immunology, St Mary's Hospital Medical School, London, UK.
FAU - Guida, L
AU  - Guida L
FAU - Sun, Q
AU  - Sun Q
FAU - Korpelainen, E I
AU  - Korpelainen EI
FAU - van den Heuvel, C
AU  - van den Heuvel C
FAU - Gillis, D
AU  - Gillis D
FAU - Hawrylowicz, C M
AU  - Hawrylowicz CM
FAU - Vadas, M A
AU  - Vadas MA
FAU - Lopez, A F
AU  - Lopez AF
LA  - eng
GR  - Wellcome Trust/United Kingdom
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Blood
JT  - Blood
JID - 7603509
RN  - 0 (HLA-D Antigens)
RN  - 0 (Interleukin-3)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Granulocyte-Macrophage Colony-Stimulating Factor)
RN  - 0 (Receptors, Interleukin-3)
RN  - 0 (Recombinant Proteins)
RN  - 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor)
SB  - IM
MH  - Cells, Cultured
MH  - Flow Cytometry
MH  - Gene Expression Regulation/*drug effects
MH  - Granulocyte-Macrophage Colony-Stimulating Factor/*pharmacology
MH  - HLA-D Antigens/*biosynthesis/genetics
MH  - Humans
MH  - Interleukin-3/metabolism/*pharmacology
MH  - Neutrophil Activation/*drug effects
MH  - Neutrophils/*drug effects/immunology/metabolism
MH  - RNA, Messenger/biosynthesis
MH  - Receptors, Granulocyte-Macrophage Colony-Stimulating 
      Factor/analysis/biosynthesis/genetics
MH  - Receptors, Interleukin-3/analysis/biosynthesis/genetics/*physiology
MH  - Recombinant Proteins/*pharmacology
MH  - Signal Transduction
EDAT- 1995/11/15 00:00
MHDA- 1995/11/15 00:01
CRDT- 1995/11/15 00:00
PHST- 1995/11/15 00:00 [pubmed]
PHST- 1995/11/15 00:01 [medline]
PHST- 1995/11/15 00:00 [entrez]
AID - S0006-4971(20)63249-9 [pii]
PST - ppublish
SO  - Blood. 1995 Nov 15;86(10):3938-44.