Endothelial Interferon Regulatory Factor 1 Cooperates with NF-κB as a Transcriptional Activator of Vascular Cell Adhesion Molecule 1

Neish, Andrew S.; Read, Margaret; Thanos, Dimitris; Pine, Richard; Maniatis, Tom; Collins, Tucker

doi:10.1128/mcb.15.5.2558

Cited by 284 publications

(231 citation statements)

References 68 publications

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“…12A provide evidence that HMG-I(Y) is a constituent of the other major complex which binds in the positive regulatory domain of Qp. Qp is thus similar to the IFN-␤ and VCAM-1 promoters, which have binding sites for HMG-I(Y) and IRF1-IRF2 (53,82,84). As shown in Fig.…”

Section: Discussionmentioning

confidence: 78%

Constitutive Activation of Epstein-Barr Virus (EBV) Nuclear Antigen 1 Gene Transcription by IRF1 and IRF2 during Restricted EBV Latency

Schaefer

Paulson

Strominger

et al. 1997

Molecular and Cellular Biology

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Epstein-Barr virus (EBV) infection in immunocompetenthumans is predominantly latent and persists for the life of the individual (reviewed in reference 41). Recently, it has been shown that EBV is capable of adopting at least three distinct forms of latency (27). Type III latency is observed upon in vitro infection of B lymphocytes and results in immortalization and continuous proliferation of the infected B cells via the action of a subset of the six EBV nuclear antigens (EBNAs; EBNA1, EBNA2, EBNA3a, EBNA3b, EBNA3c, and EBNA4) and three membrane proteins (LMP1, LMP2a, and LMP2b) expressed in the type III (immortalizing) program. However, in vivo, the type III latency program is likely to be only transiently observed upon initial infection of a naive host, since several of the type III latent antigens elicit a potent cytotoxic T-lymphocyte response resulting in very effective elimination of type III latently infected B cells (reviewed in reference 33).EBV is also capable of entering programs of latency in which the expression of latent antigens is restricted with respect to the type III program. In type I latency, only the EBNA1 protein is expressed (64). It has recently been shown that EBNA1 peptides do not enter the major histocompatibility complex class I antigen processing and presentation pathway (29, 39, 52), and cells which express only EBNA1 are not detected by host cellular immune surveillance mechanisms (63). The type II latency program differs from type I latency only in the expression of variable combinations of LMP1, LMP2a, and LMP2b, in addition to EBNA1. Since the type I latency program was identified, there has been speculation that type I latently infected B lymphocytes represent the lifelong reservoir of virus in immunocompetent, seropositive individuals, and there have recently been several reports which provide evidence that a type I-like form of restricted viral latency does indeed exist in healthy carriers of EBV (6,51,60,85).Investigations into the molecular basis of type III and type I latency have demonstrated that distinct promoters are used to drive transcription of the EBNAs in each latent program. In type III latency, transcription of all six nuclear antigens is initiated from either Wp (during initial infection of resting B cells) or Cp (in cycling B cells), and the long primary transcripts are differentially spliced to generate the mature EBNA transcripts (75, 94; see Fig. 1A for a schematic representation of EBV latent transcription and locations of promoters). Recent investigations have shown that transcription of the EBNA1 gene in type I latency is driven by a promoter designated Qp, which is considerably downstream of the type III latency EBNA gene promoters (57,(70)(71)(72). Qp has an architecture with numerous similarities to eukaryotic housekeeping

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Section: Discussionmentioning

confidence: 78%

Constitutive Activation of Epstein-Barr Virus (EBV) Nuclear Antigen 1 Gene Transcription by IRF1 and IRF2 during Restricted EBV Latency

Schaefer

Paulson

Strominger

et al. 1997

Molecular and Cellular Biology

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“…This hetero-dimerization would be mediated by DNA binding, as IRFs exist as monomers in solution . In several other cases, synergistic activation of a promoter has been explained by the increase in promoter element binding induced by the physical interaction between two transcription factors (Pongubala et al, 1993;Eisenbeis et al, 1995;Neish et al, 1995;Sun et al, 1995;Pongubala and Atchison, 1997). For example, IRF-1 and NF-kB synergistically activate the endothelial VCAM-1 through physical interaction of IRF-1 with the p50 subunit of NF-kB (Neish et al, 1995).…”

Section: Discussionmentioning

confidence: 99%

Co-occupancy of the interferon regulatory element of the class II transactivator (CIITA) Type IV promoter by interferon regulatory factors 1 and 2

Eason

Ghosh

et al. 1999

Oncogene

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“…Given that expression of many IFN-g-responsive chemokines were induced only upon costimulation with IFN-g and cagPAI + H. pylori bacteria, we next investigated the expression of the transcription factor, IRF1, which can be upregulated by both STAT1 (28) and NF-kB (46,47). qRT-PCR analysis revealed strong IRF1 expression in cells stimulated with H. pylori WT and DcagA mutant, although not DcagM, bacteria within 2 h (Fig.…”

Section: H Pylori Induces Irf1 Transcription In a Cagpai-and Nod1-dementioning

confidence: 99%

Nucleotide Oligomerization Domain 1 Enhances IFN-γ Signaling in Gastric Epithelial Cells during Helicobacter pylori Infection and Exacerbates Disease Severity

Allison

Ferrand

McLeod

et al. 2013

The Journal of Immunology

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Virulent Helicobacter pylori strains that specifically activate signaling in epithelial cells via the innate immune molecule, nucleotide oligomerization domain 1 (NOD1), are more frequently associated with IFN-γ–dependent inflammation and with severe clinical outcomes (i.e., gastric cancer and peptic ulceration). In cell culture models, we showed that H. pylori activation of the NOD1 pathway caused enhanced proinflammatory signaling in epithelial cells in response to IFN-γ stimulation through the direct effects of H. pylori on two components of the IFN-γ signaling pathway, STAT1 and IFN regulatory factor 1 (IRF1). Specifically, H. pylori activation of the NOD1 pathway was shown to increase the levels of STAT1-Tyr701/Ser727 phosphorylation and IRF1 expression/synthesis in cells, resulting in enhanced production of the NOD1- and IFN-γ–regulated chemokines, IL-8– and IFN-γ–induced protein 10, respectively. Consistent with the notion that heightened proinflammatory signaling in epithelial cells may have an impact on disease severity, we observed significantly increased expression levels of NOD1, CXCL8, IRF1, and CXCL10 in human gastric biopsies displaying severe gastritis, when compared with those without gastritis (p < 0.05, p < 0.001, p < 0.01, and p < 0.05, respectively). Interestingly, NOD1, CXCL8, and IRF1 expression levels were also significantly upregulated in gastric tumor tissues, when compared with paired nontumor samples (p < 0.0001, p < 0.05, and p < 0.05, respectively). Thus, we propose that cross-talk between NOD1 and IFN-γ signaling pathways contribute to H. pylori–induced inflammatory responses, potentially revealing a novel mechanism whereby virulent H. pylori strains promote more severe disease.

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Endothelial Interferon Regulatory Factor 1 Cooperates with NF-κB as a Transcriptional Activator of Vascular Cell Adhesion Molecule 1

Cited by 284 publications

References 68 publications

Constitutive Activation of Epstein-Barr Virus (EBV) Nuclear Antigen 1 Gene Transcription by IRF1 and IRF2 during Restricted EBV Latency

Constitutive Activation of Epstein-Barr Virus (EBV) Nuclear Antigen 1 Gene Transcription by IRF1 and IRF2 during Restricted EBV Latency

Co-occupancy of the interferon regulatory element of the class II transactivator (CIITA) Type IV promoter by interferon regulatory factors 1 and 2

Nucleotide Oligomerization Domain 1 Enhances IFN-γ Signaling in Gastric Epithelial Cells during Helicobacter pylori Infection and Exacerbates Disease Severity

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