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Departments of 1 Pediatrics, 2 Microbiology and Immunology, and 3 Internal Medicine and 4 Sealy Center for Molecular Sciences, University of Texas Medical Branch, Galveston, Texas 77555
Regulated on activation, normal T cell
expressed, and presumably secreted (RANTES) is a member of the CC
chemokine family of proteins implicated in a variety of diseases
characterized by lung eosinophilia and inflammation, strongly produced
by stimulated airway epithelial cells. Because such cytokines as tumor
necrosis factor (TNF)-
and interferon-
(IFN-) have been shown
to enhance RANTES induction in airway epithelial cells and RANTES gene
expression appears to be differentially regulated depending on the cell
type and the stimulus applied, in this study we have elucidated
mechanisms that operate to control RANTES induction on exposure to
TNF- and/or IFN-. Our results indicate that TNF- and IFN-
synergistically induce RANTES protein secretion and mRNA expression.
RANTES transcription is activated only after stimulation with TNF-,
but not IFN-, which affects RANTES mRNA stabilization. Promoter
deletion and mutagenesis experiments indicate that the nuclear factor
(NF)-
B site is the most important cis-regulatory element
controlling TNF-induced RANTES transcription, although NF-interleukin-6
binding site, cAMP responsive element (CRE), and interferon-stimulated responsive element (ISRE) also play a significant role. TNF- stimulation induces nuclear translocation of interferon regulatory factor (IRF)-3, which in viral infection binds the RANTES ISRE and is
necessary for activation of RANTES transcription. However, TNF-induced
IRF-3 translocation does not result in IRF-3 binding to the RANTES
ISRE. Although viral infection can activate an ISRE-driven promoter,
TNF cannot, indicating that RANTES gene enhancers are controlled in a
stimulus-specific fashion. Identification of molecular mechanisms
involved in RANTES gene expression is fundamental for developing
strategies to modulate lung inflammatory responses.
tumor necrosis factor; interferon; nuclear factor-B; regulated
on activation, normal T cell expressed, and presumably secreted
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