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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
Author(s) -
HASHIMOTO S.,
GON Y.,
HAYASHI S.,
TOMITA Y.,
YODOI J.,
HORIE T.
Publication year - 1997
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1046/j.1365-3083.1997.d01-396.x
Subject(s) - cd23 , immunology , chemistry , tumor necrosis factor alpha , microbiology and biotechnology , medicine , immunoglobulin e , biology , antibody
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.