TNF-α Regulates GM-CSF-, IL-3- or M-CSF-Induced Fc ε RII/CD23 Gene Expression and Soluble Fc ε RII Release by Human Monocytes
HASHIMOTO, S. ; GON, Y. ; HAYASHI, S. ; TOMITA, Y. ; YODOI, J. ; HORIE, T.
Oxford, U.K. and Cambridge, USA : Blackwell Science Ltd
Published 1997
Oxford, U.K. and Cambridge, USA : Blackwell Science Ltd
Published 1997
ISSN: |
1365-3083
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Source: |
Blackwell Publishing Journal Backfiles 1879-2005
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Topics: |
Medicine
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Notes: |
The authors examined the regulatory effects of tumour necrosis factor-α (TNF-α) on granulocyte macrophage colony stimulating factor (GM-CSF)-, interleukin-3 (IL-3)- or macrophage colony stimulating factor (M-CSF)-induced gene expression of the low affinity receptor for IgE (Fc ε RII) on human monocytes and GM-CSF-, IL-3- or M-CSF-induced soluble Fc ε RII (sFc ε RII) release from monocytes. The expression of GM-CSF-, IL-3- or M-CSF-induced Fc ε RII on the surface of monocytes was reduced by TNF-α. The present analysis was designed to examine whether or not TNF-α could suppress GM-CSF-, IL-3- or M-CSF-induced Fc ε RII messenger RNA (mRNA) expression and enhance the release of sFc ε RII induced by these cytokines. The addition of TNF-α to monocyte cultures with GM-CSF, IL-3 or M-CSF significantly reduced Fc ε RII expression on the surface of monocytes and significantly increased sFc ε RII release from monocytes. These results suggest that TNF-α-dependent reduction of GM-CSF-, IL-3- or M-CSF-induced Fc ε RII expression on the surface of monocytes resulted, at least in part, from the suppression of Fc ε RII mRNA and the enhancement of sFc ε RII release.
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Type of Medium: |
Electronic Resource
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URL: |