TNF-alpha regulates GM-CSF-, IL-3- or M-CSF-induced Fc epsilon RII/CD23 gene expression and soluble Fc epsilon RII release by human monocytes.

Abstract

The authors examined the regulatory effects of tumour necrosis factor-alpha (TNF-alpha) 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 epsilon RII) on human monocytes and GM-CSF-, IL-3- or M-CSF-induced soluble Fc epsilon RII (sFc epsilon RII) release from monocytes. The expression of GM-CSF-, IL-3- or M-CSF-induced Fc epsilon RII on the surface of monocytes was reduced by TNF-alpha. The present analysis was designed to examine whether or not TNF-alpha could suppress GM-CSF-, IL-3- or M-CSF-induced Fc epsilon RII messenger RNA (mRNA) expression and enhance the release of sFc epsilon RII induced by these cytokines. The addition of TNF-alpha to monocyte cultures with GM-CSF, IL-3 or M-CSF significantly reduced Fc epsilon RII expression on the surface of monocytes and significantly increased sFc epsilon RII release from monocytes. These results suggest that TNF-alpha-dependent reduction of GM-CSF-, IL-3- or M-CSF-induced Fc epsilon RII expression on the surface of monocytes resulted, at least in part, from the suppression of Fc epsilon RII mRNA and the enhancement of sFc epsilon RII release.