Regulation of RANTES Chemokine Gene Expression Requires Cooperativity Between NF-κB and IFN-Regulatory Factor Transcription Factors

Génin, Pierre; Algarté, Michèle; Roof, Philippe; Lin, Rongtuan; Hiscott, John

doi:10.4049/jimmunol.164.10.5352

Cited by 206 publications

(220 citation statements)

References 43 publications

(46 reference statements)

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“…Expression of RANTES requires cooperative effect between NF-B and IRF3/7 (40). The near complete inhibition of RANTES in TRIF-deficient macrophages and mice lung is likely due to an impaired NF-B activation because IRF activation was not observed after P. aeruginosa infection in this study.…”

Section: Figurementioning

confidence: 56%

A Role of Toll-IL-1 Receptor Domain-Containing Adaptor-Inducing IFN-β in the Host Response to Pseudomonas aeruginosa Lung Infection in Mice

Power¹,

Li²,

Yamamoto

et al. 2007

The Journal of Immunology

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Toll-IL-1R domain-containing adaptor-inducing IFN-β (TRIF) is an adaptor molecule that mediates a distinct TLR signaling pathway. Roles of TRIF in the host defense have been primarily associated with virus infections owing to the induction of IFN-αβ. In this study, we investigated a role of TRIF in Pseudomonas aeruginosa infection. In vitro, TRIF-deficient mouse alveolar and peritoneal macrophages showed a complete inhibition of RANTES (CCL5) production, severely impaired TNF and KC (CXCL1) production, and reduced NF-κB activation in response to P. aeruginosa stimulation. In vivo, TRIF-deficient mice showed a complete inhibition of RANTES production, a severely impaired TNF and KC production, and an efficient MIP-2 and IL-1β production in the lung following P. aeruginosa infection. This outcome was associated with a delayed recruitment of neutrophils into the airways. These results suggest that TRIF mediates a distinct cytokine/chemokine profile in response to P. aeruginosa infection. P. aeruginosa-induced RANTES production is completely dependent on TRIF pathway in mice. Importantly, TRIF deficiency leads to impaired clearance of P. aeruginosa from the lung during the initial 24–48 h of infection. Thus, TRIF represents a novel mechanism involved in the development of host response to P. aeruginosa infection.

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Section: Figurementioning

confidence: 56%

A Role of Toll-IL-1 Receptor Domain-Containing Adaptor-Inducing IFN-β in the Host Response to Pseudomonas aeruginosa Lung Infection in Mice

Power¹,

Li²,

Yamamoto

et al. 2007

The Journal of Immunology

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“…IRF-7 and IRF-3 (not found as modified in the array; data not shown) play critical roles in the innate response to a viral infection [53] and IRF-7 also contributes to IFN-γ-mediated apoptosis [55]. Among the downstream genes regulated by IRF-7, in cooperation with NF-κB, is the CC chemokine RANTES [56]. We observed that PIC increased RANTES expression by more than 100-fold.…”

Section: Discussionmentioning

confidence: 75%

Global profiling of double stranded RNA- and IFN-?-induced genes in rat pancreatic beta cells

et al. 2003

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Aims/hypothesis. Viral infections and local production of IFN-γ might contribute to beta-cell dysfunction/ death in Type 1 Diabetes. Double stranded RNA (dsRNA) accumulates in the cytosol of viral-infected cells, and exposure of purified rat beta cells to dsRNA (tested in the form of polyinosinic-polycytidylic acid, PIC) in combination with IFN-γ results in beta-cell dysfunction and apoptosis. To elucidate the molecular mechanisms involved in PIC + IFN-γ-effects, we determined the global profile of genes modified by these agents in primary rat beta cells. Methods. FACS-purified rat beta cells were cultured for 6 or 24 h in control condition or with IFN-γ, PIC or a combination of both agents. The gene expression profile was analysed in duplicate by high-density oligonucleotide arrays representing 5000 full-length genes and 3000 EST's. Changes of greater than or equal to 2.5-fold were considered as relevant.Results. Following a 6-or 24-h treatment with IFN-γ, PIC or IFN-γ and PIC, we observed changes in the expression of 51 to 189 genes. IFN-γ modified the expression of MHC-related genes, and also of genes involved in beta-cell metabolism, protein processing, cytokines and signal transduction. PIC affected preferentially the expression of genes related to cell adhesion, cytokines and dsRNA signal transduction, transcription factors and MHC. PIC and/or IFN-γ up-regulated the expression of several chemokines and cytokines that could contribute to mononuclear cell homing and activation during viral infection, while IFN-γ induced a positive feedback on its own signal transduction. PIC + IFN-γ inhibited insulin and GLUT-2 expression without modifying pdx-1 mRNA expression. Conclusion/interpretation. This study provides the first comprehensive characterization of the molecular responses of primary beta cells to dsRNA + IFN-γ, two agents that are probably present in the beta cell milieu during the course of virally-induced insulitis and Type 1 Diabetes. Based on these findings, we propose an integrated model for the molecular mechanisms involved in dsRNA + IFN-γ induced beta-cell dysfunction and death. [Diabetologia (2003[Diabetologia ( ) 46:1641[Diabetologia ( -1657

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“…hTERT-HME1-derived cells, untreated or treated with TNF-␣ for 4 h, were lysed in EMSA lysis buffer, supplemented with protease inhibitors. The probe was the NF B consensus sequence (top strand, 5Ј-TTTTGGAAACTCCCCTTAGGGGA TGCCCCT-3Ј) from the RANTES promoter (Nelson et al 1993;Genin et al 2000). Labeled probe (10 4 DPM) was used in each binding reaction.…”

Section: Emsasmentioning

confidence: 99%

Unphosphorylated STAT3 accumulates in response to IL-6 and activates transcription by binding to NFκB

Yang¹,

Liao²,

Agarwal³

et al. 2007

Genes Dev.

546

496

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Regulation of RANTES Chemokine Gene Expression Requires Cooperativity Between NF-κB and IFN-Regulatory Factor Transcription Factors

Cited by 206 publications

References 43 publications

A Role of Toll-IL-1 Receptor Domain-Containing Adaptor-Inducing IFN-β in the Host Response to Pseudomonas aeruginosa Lung Infection in Mice

A Role of Toll-IL-1 Receptor Domain-Containing Adaptor-Inducing IFN-β in the Host Response to Pseudomonas aeruginosa Lung Infection in Mice

Global profiling of double stranded RNA- and IFN-?-induced genes in rat pancreatic beta cells

Unphosphorylated STAT3 accumulates in response to IL-6 and activates transcription by binding to NFκB

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