IL-18 receptor expression on epithelial cells is upregulated by TNF alpha
Language English Country United States Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
- MeSH
- Enzyme-Linked Immunosorbent Assay MeSH
- Epithelial Cells drug effects MeSH
- Interleukin-18 genetics pharmacology MeSH
- Interleukin-8 metabolism MeSH
- Humans MeSH
- Cell Line, Tumor MeSH
- Reverse Transcriptase Polymerase Chain Reaction MeSH
- Flow Cytometry MeSH
- Interleukin-18 Receptor alpha Subunit MeSH
- Receptors, Interleukin-18 MeSH
- Receptors, Interleukin metabolism MeSH
- Recombinant Proteins pharmacology MeSH
- Tumor Necrosis Factor-alpha pharmacology MeSH
- Up-Regulation drug effects MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- IL18R1 protein, human MeSH Browser
- Interleukin-18 MeSH
- Interleukin-8 MeSH
- Interleukin-18 Receptor alpha Subunit MeSH
- Receptors, Interleukin-18 MeSH
- Receptors, Interleukin MeSH
- Recombinant Proteins MeSH
- Tumor Necrosis Factor-alpha MeSH
IL-18 is a multifunctional cytokine that augments both innate and acquired immunity and potentiates Th1 and Th2 reactions. We studied the expression of IL-18 receptor (IL-18R) on renal and respiratory epithelial cell lines. Both cell lines upregulated IL-18R mRNA and IL-18R membrane expression in response to TNF alpha and other proinflammatory cytokines. The function of IL-18R was confirmed by induction of IL-8 release from epithelial cells in response to recombinant IL-18. Epithelial cells may represent an important target for IL-18, mainly under inflammatory conditions associated with TNF alpha release.
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