p38 activation through Toll-like receptors modulates IFN-γ-induced expression of the Tap-1 gene only in macrophages
| Autor: | Alicia Cecil, Michael J. Klemsz |
|---|---|
| Rok vydání: | 2003 |
| Předmět: |
Immunology
Receptors Cell Surface Biology p38 Mitogen-Activated Protein Kinases Cell Line Major Histocompatibility Complex Interferon-gamma Humans Immunology and Allergy ATP Binding Cassette Transporter Subfamily B Member 2 Phosphorylation Receptor Transcription factor Regulation of gene expression Membrane Glycoproteins Activator (genetics) Macrophages Toll-Like Receptors Drug Synergism Cell Biology Molecular biology Toll-Like Receptor 2 Cell biology DNA-Binding Proteins Toll-Like Receptor 4 TLR2 STAT1 Transcription Factor Gene Expression Regulation Toll-Like Receptor 9 Trans-Activators TLR4 ATP-Binding Cassette Transporters Mitogen-Activated Protein Kinases Signal transduction HeLa Cells Signal Transduction |
| Zdroj: | Journal of Leukocyte Biology. 75:560-568 |
| ISSN: | 1938-3673 0741-5400 |
| DOI: | 10.1189/jlb.0803375 |
| Popis: | Although interferon-γ (IFN-γ) induces the transporter associated with antigen processing (Tap)-1 expression in macrophages, cooperation with lipopolysaccharide signaling through Toll-like receptor 4 (TLR4) accelerates the kinetics and increases the overall levels of this gene. In this report, we show that peptidoglycan signaling through TLR2 and bacterial CpG DNA signaling through TLR9 are functionally equivalent at synergizing with IFN-γ in regulating Tap-1 expression in macrophages. Activation of the p38 mitogen-activated protein kinase is necessary for this response, which correlates with increased phosphorylation of signal transducer and activator of transcription-1 on serine 727. Activation of p38, however, is not sufficient, as this signaling event does not affect the response to IFN-γ in HeLa cells. The cooperation between these different signaling pathways also requires membrane fluidity. These data suggest that macrophages possess an ability to coordinate the signaling between the IFN-γ and TLR receptors. |
| Databáze: | OpenAIRE |
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