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Published online before print December 23, 2003

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(Journal of Leukocyte Biology. 2004;75:560-568.)
© 2004 by Society for Leukocyte Biology

p38 activation through Toll-like receptors modulates IFN--induced expression of the Tap-1 gene only in macrophages

Department of Microbiology and Immunology, Indiana University School of Medicine and the Walther Cancer Institute, Indianapolis

² Correspondance: Department of Microbiology and Immunology, Indiana University School of Medicine, 635 Barnhill Dr., MS5010, Indianapolis, IN 46202. E-mail: mklemsz{at}iupui.edu

Although interferon- (IFN-) 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- 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- 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- and TLR receptors.

Key Words: gene regulation • transcription factor • macrophages

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