An association study of functional polymorphic genes IRF-1, IFNGR-1, and IFN-γ with disease progression, aspartate aminotransferase, alanine aminotransferase, and viral load in chronic hepatitis B and C

Korachi, May; Ceran, Nurgül; Adaleti, Rıza; Niğdelioğlu, Adil; Sokmen, Mehmet

doi:10.1016/j.ijid.2012.08.004

Cited by 27 publications

(30 citation statements)

References 34 publications

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“…Utilizing this advanced technology, the preliminary clinical relevance of IRFs has been established. A recent study observed that IRF1, at positions -388 and -410, might be a candidate gene marker for chronic hepatitis B and C (Korachi et al, 2013). Applying genome-wide SNP association study, Di Bernardo et al (2008) demonstrated that IRF4 is strongly associated with susceptibility to chronic lymphocytic leukaemia (CLL).…”

Section: Potential Clinical Applications Of Irfsmentioning

confidence: 99%

“…In the C-terminal region, the IRFs, except for IRF1 and IRF2, contain IAD1, while IRF1 and IRF2 share IAD2. Liu et al, 2000;Taniguchi et al, 2001;Watford et al, 2003;Wessely et al, 2003;Mellor and Munn, 2004;Passioura et al, 2005;Tamura et al, 2005;Caso et al, 2007;Schmitz et al, 2007;Li et al, 2009;Korachi et al, 2013;Jiang et al, 2014a IRF2 Taniguchi et al, 2001;Ichikawa et al, 2004;Jia and Guo, 2008 IRF3 Most cell types and organs Dilated cardiomyopathy, hypertrophic cardiomyopathy, stroke, AS, AAA Induces type I IFNs; reduces cardiac hypertrophy; indispensable for TLR ligands pretreatment-induced tolerance to stroke;…”

Section: Figurementioning

confidence: 99%

“…In the C-terminal region, the IRFs, except for IRF1 and IRF2, contain IAD1, while IRF1 and IRF2 share IAD2. Liu et al, 2000;Taniguchi et al, 2001;Watford et al, 2003;Wessely et al, 2003;Mellor and Munn, 2004;Passioura et al, 2005;Tamura et al, 2005;Caso et al, 2007;Schmitz et al, 2007;Li et al, 2009;Korachi et al, 2013;Jiang et al, 2014a IRF2 IL-4, CREB, SRF Pernis, 2002;Schiavoni et al, 2002;Lehtonen et al, 2003;Kanno et al, 2005;Negishi et al, 2005;Tamura et al, 2005;Di Bernardo et al, 2008;Jiang et al, 2013;Pinto et al, 2013;Guo et al, 2014 IRF5 Lehtonen et al, 2003;…”

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The interferon regulatory factors as novel potential targets in the treatment of cardiovascular diseases

Zhang

Jiang

2015

British J Pharmacology

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The family of interferon regulatory factors (IRFs) consists of nine members (IRF1-IRF9) in mammals. They act as transcription factors for the interferons and thus exert essential regulatory functions in the immune system and in oncogenesis. Recent clinical and experimental studies have identified critically important roles of the IRFs in cardiovascular diseases, arising from their participation in divergent and overlapping molecular programmes beyond the immune response. Here we review the current knowledge of the regulatory effects and mechanisms of IRFs on the immune system. The role of IRFs and their potential molecular mechanisms as novel stress sensors and mediators of cardiovascular diseases are highlighted. LINKED ARTICLESThis article is part of a themed section on Chinese Innovation in Cardiovascular Drug Discovery. To view the other articles in this section visit http://dx.doi. org/10.1111/bph.2015.172.issue-23 Abbreviations ATF3, activating transcription factor 3; CBP, CREB-binding protein; cDCs, conventional dendritic cells; CLL, chronic lymphocytic leukaemia; CMPs, common myeloid progenitor cells; CREB, cAMP-responsive element-binding protein; Dock2, dedicator of cytokinesis 2; dsRNA, double-stranded RNA; ECM, extracellular matrix; ET-1, endothelin-1; GSK3β, glycogen synthase kinase 3β; GWAS, genome-wide association studies; HATs, histone acetyltransferases; HDACs, histone deacetylases; I/R, ischaemia/reperfusion; IAD, IRF-associated domain; IFN, interferon ; IGF-I, insulin-like growth factor I; iNOS, inducible NOS; IRFs, interferon regulatory factors; MAVS, mitochondrial antiviral signalling protein; MDA5, melanoma differentiation-associated gene 5; MyD88, myeloid differentiation primary-response protein 88; PCAF, p300/CBP-associated factor; pDCs, plasma cytoid dendritic cells; PRR, pattern recognition receptor; RIG-I, retinoic acid-inducible gene I; SLE, systemic lupus erythematosus; SRF, serum response factor; TAD, transcription activation domain; TBK1, TANK-binding kinase 1; TG, transgene; TIRAP, TIR domain-containing adaptor protein; TLRs, Toll-like receptors; TRAF, TNF receptor-associated factor; TRAM, TRIF-related adaptor molecule; TRIF, TIRAP-inducing IFN-β; Tyk2, tyrosine kinase 2; VSMCs, vascular smooth muscle cells Tables of Links Introduction and backgroundThe interferon regulatory factor (IRF) family was first described as transcriptional regulators of the type I interferon (IFN) system. Since 1988, when the first IRF was identified (Miyamoto et al., 1988), most studies of IRFs have focused on their functions in immunity. Abnormalities in IRFs are associated with changes in both innate and adaptive immune responses to cellular and environmental stimuli in a wide variety of pathways. Now, more recent evidence has revealed the remarkable contributions of IRFs to other diseases, such as cardiovascular diseases Jiang et al., 2014d;Zhang et al., 2014a), metabolic diseases (Eguchi et al., 2008;2011; Wang et al., 2013c,d;2014) and oncogenesis (Yanai et al., 2012). In this review, as docume...

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Section: Potential Clinical Applications Of Irfsmentioning

confidence: 99%

Section: Figurementioning

confidence: 99%

“…In the C-terminal region, the IRFs, except for IRF1 and IRF2, contain IAD1, while IRF1 and IRF2 share IAD2. Liu et al, 2000;Taniguchi et al, 2001;Watford et al, 2003;Wessely et al, 2003;Mellor and Munn, 2004;Passioura et al, 2005;Tamura et al, 2005;Caso et al, 2007;Schmitz et al, 2007;Li et al, 2009;Korachi et al, 2013;Jiang et al, 2014a IRF2 IL-4, CREB, SRF Pernis, 2002;Schiavoni et al, 2002;Lehtonen et al, 2003;Kanno et al, 2005;Negishi et al, 2005;Tamura et al, 2005;Di Bernardo et al, 2008;Jiang et al, 2013;Pinto et al, 2013;Guo et al, 2014 IRF5 Lehtonen et al, 2003;…”

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The interferon regulatory factors as novel potential targets in the treatment of cardiovascular diseases

Zhang

Jiang

2015

British J Pharmacology

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“…However, there is a paucity of studies defining the role of IRF-1 during chronic virus infection. Such a role undoubtedly exists, as distinct IRF-1 polymorphisms are associated with either susceptibility to chronic hepatitis B and C virus infection (6) or resistance to HIV-1 (7). Additionally, IRF-1 is a tumor suppressor, as evidenced by the synergy between IRF-1 insufficiency and oncogene deregulation in animal models (8) and decreased IRF-1 expression in several human cancers (9).…”

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confidence: 99%

Tumor Suppressor Interferon-Regulatory Factor 1 Counteracts the Germinal Center Reaction Driven by a Cancer-Associated Gammaherpesvirus

Mboko

Olteanu

Ray

et al. 2016

J Virol

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Gammaherpesviruses are ubiquitous pathogens that are associated with the development of B cell lymphomas. Gammaherpesviruses employ multiple mechanisms to transiently stimulate a broad, polyclonal germinal center reaction, an inherently mutagenic stage of B cell differentiation that is thought to be the primary target of malignant transformation in virus-driven lymphomagenesis. We found that this gammaherpesvirus-driven germinal center expansion was exaggerated and lost its transient nature in the absence of interferon-regulatory factor 1 (IRF-1), a transcription factor with antiviral and tumor suppressor functions. Uncontrolled and persistent expansion of germinal center B cells led to pathological changes in the spleens of chronically infected IRF-1-deficient animals. Additionally, we found decreased IRF-1 expression in cases of human posttransplant lymphoproliferative disorder, a malignant condition associated with gammaherpesvirus infection. The results of our study define an unappreciated role for IRF-1 in B cell biology and provide insight into the potential mechanism of gammaherpesvirus-driven lymphomagenesis. IMPORTANCE Gammaherpesviruses establish lifelong infection in most adults and are associated with B cell lymphomas. While the infection is asymptomatic in many hosts, it is critical to identify individuals who may be at an increased risk of virus-induced cancer. Such identification is currently impossible Interferon-regulatory factor 1 (IRF-1) is a conserved transcription factor that restricts the replication of diverse RNA and DNA viruses in vitro via a poorly understood mechanism (1, 2). Additionally, IRF-1 suppresses replication and restricts the tropism of West Nile virus (WNV) (3), vesicular stomatitis virus (VSV) (4), and murine norovirus (5) during the acute phase of infection in vivo. However, there is a paucity of studies defining the role of IRF-1 during chronic virus infection. Such a role undoubtedly exists, as distinct IRF-1 polymorphisms are associated with either susceptibility to chronic hepatitis B and C virus infection (6) or resistance to HIV-1 (7). Additionally, IRF-1 is a tumor suppressor, as evidenced by the synergy between IRF-1 insufficiency and oncogene deregulation in animal models (8) and decreased IRF-1 expression in several human cancers (9). Importantly, this tumor suppressor nature of IRF-1 may be of particular relevance in the context of chronic infection with cancer-associated viruses.Our study focuses on the interaction between IRF-1 and gammaherpesviruses, ubiquitous pathogens that establish lifelong infection in a majority of the human population and are associated with the development of B cell lymphomas (10). In spite of the widespread nature of gammaherpesvirus infection, the host risk factors that predispose individuals toward gammaherpesvirus-driven lymphomagenesis are still poorly understood. Gammaherpesviruses establish long-term latency in memory B cells. Accordingly, these viruses employ both viral and host mechanisms to stimulate a germinal cent...

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“…IRF1 has been shown to play roles in regulating apoptosis, tumor-suppression and DNA damage response [71,72]. Findings suggest that IRF1 is a candidate gene marker for determining patient susceptibility to the development of chronic hepatitis B and C [73,74]. Some findings indicate that a common mis-sense SNP in ATF6 may contribute to susceptibility of HCC functionally [75].…”

Section: Discussionmentioning

confidence: 99%

Identification of the transcriptional regulators by expression profiling infected with hepatitis B virus

Chai

Han

Yang

et al. 2016

Clinics and Research in Hepatology and Gastroenterology

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An association study of functional polymorphic genes IRF-1, IFNGR-1, and IFN-γ with disease progression, aspartate aminotransferase, alanine aminotransferase, and viral load in chronic hepatitis B and C

Abstract: Findings suggest that IFN-γ (+874), IRF-1 (-410, -388), and IFNGR-1 (-56, -611) are candidate gene markers for determining patient susceptibility to the development of chronic hepatitis B and C.

Cited by 27 publications

References 34 publications

The interferon regulatory factors as novel potential targets in the treatment of cardiovascular diseases

The interferon regulatory factors as novel potential targets in the treatment of cardiovascular diseases

Tumor Suppressor Interferon-Regulatory Factor 1 Counteracts the Germinal Center Reaction Driven by a Cancer-Associated Gammaherpesvirus

Identification of the transcriptional regulators by expression profiling infected with hepatitis B virus

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