scholarly journals Interferon regulatory factor 1 inactivation in human cancer

2018 ◽  
Vol 38 (3) ◽  
Author(s):  
Khaldoon Alsamman ◽  
Omar S. El-Masry
Keyword(s):  
Inflammatory Responses ◽  
Current Knowledge ◽  
Human Cancer ◽  
Tumor Biology ◽  
Interferon Regulatory Factor ◽  
Potential Importance ◽  
Regulatory Factor ◽  
Interferon Regulatory Factor 1 ◽  
Related Proteins ◽  
The Impact

Interferon regulatory factors (IRFs) are a group of closely related proteins collectively referred to as the IRF family. Members of this family were originally recognized for their roles in inflammatory responses; however, recent research has suggested that they are also involved in tumor biology. This review focusses on current knowledge of the roles of IRF-1 and IRF-2 in human cancer, with particular attention paid to the impact of IRF-1 inactivation. The different mechanisms underlying IRF-1 inactivation and their implications for human cancers and the potential importance of IRF-1 in immunotherapy are also summarized.

scholarly journals Prevention of lymphocytic thyroiditis in iodide-treated non-obese diabetic mice lacking interferon regulatory factor-1

2002 ◽  
pp. 809-814 ◽  
Author(s):  
J Tani ◽  
K Mori ◽  
S Hoshikawa ◽  
T Nakazawa ◽  
J Satoh ◽  
...  
Keyword(s):  
Nod Mice ◽  
Interleukin 10 ◽  
Interferon Regulatory Factor ◽  
Enzyme Linked Immunosorbent Assay ◽  
Regulatory Factor ◽  
Lymphocytic Thyroiditis ◽  
Water Group ◽  
Interferon Regulatory Factor 1 ◽  
Group 2 ◽  
Group 1

OBJECTIVE: Interferon regulatory factor-1 (IRF-1) is a critical regulator of interferon-gamma(IFNgamma)-mediated immune responses. To determine whether IRF-1 is involved in the pathogenesis of thyroiditis in animal models, we evaluated the incidence of iodide-induced lymphocytic thyroiditis (LT) in non-obese diabetic (NOD) mice lacking IRF-1 as well as IRF-1 +/+ and +/- mice. DESIGN: IRF-1 +/+, +/- and -/- NOD mice at 6 weeks of age were fed water (group 1) or iodide water (group 2) for 8 weeks. METHODS: Thyroids were examined histopathologically and intrathyroidal lymphocytic infiltration was arbitrarily graded. Serum thyroxine (T(4)) and anti-mouse thyroglobulin antibody (anti-mTgAb) levels were measured. Spleen cell population was analyzed by flow cytometry, and IFNgamma and interleukin-10 produced by splenocytes were measured by enzyme-linked immunosorbent assay. RESULTS: In group 1, only 4.3% of NOD mice developed LT. In contrast, 67.6% of mice in group 2 developed the disease. Iodide treatment induced LT in more than 80% of IRF-1 +/+ and +/- mice. However, no IRF-1 -/- mice in group 2 developed LT. There was no difference in both serum anti-mTgAb and T(4) levels among the three IRF-1 genotypes of NOD mice. Numbers of splenic CD8(+) T cells and IFNgamma production by Concanavalin A-stimulated splenocytes were markedly decreased in IRF-1-deficient NOD mice. CONCLUSIONS: IRF-1 is involved in the development of iodide-induced LT in NOD mice.

Interferon regulatory factor-1 promoter polymorphism and the outcome of hepatitis C virus infection

2006 ◽  
Vol 18 (9) ◽  
pp. 991-997 ◽  
Author(s):  
Perdita Wietzke-Braun ◽  
Adil B. Maouzi ◽  
Larissa B. M??nhardt ◽  
Heike Bickeb??ller ◽  
Giuliano Ramadori ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Virus Infection ◽  
Interferon Regulatory Factor ◽  
Promoter Polymorphism ◽  
Hepatitis C Virus Infection ◽  
Regulatory Factor ◽  
Interferon Regulatory Factor 1

scholarly journals Identification of Feline Interferon Regulatory Factor 1 as an Efficient Antiviral Factor against the Replication of Feline Calicivirus and Other Feline Viruses

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Yongxiang Liu ◽  
Xiaoxiao Liu ◽  
Hongtao Kang ◽  
Xiaoliang Hu ◽  
Jiasen Liu ◽  
...  
Keyword(s):  
Antiviral Activity ◽  
Viral Infections ◽  
Interferon Regulatory Factor ◽  
Feline Calicivirus ◽  
Type I ◽  
Norwalk Virus ◽  
Regulatory Factor ◽  
Feline Panleukopenia Virus ◽  
Protein Levels ◽  
Interferon Regulatory Factor 1

Interferons (IFNs) can inhibit most, if not all, viral infections by eliciting the transcription of hundreds of interferon-stimulated genes (ISGs). Feline calicivirus (FCV) is a highly contagious pathogen of cats and a surrogate for Norwalk virus. Interferon efficiently inhibits the replication of FCV, but the mechanism of the antiviral activity is poorly understood. Here, we evaluated the anti-FCV activity of ten ISGs, whose antiviral activities were previously reported. The results showed that interferon regulatory factor 1 (IRF1) can significantly inhibit the replication of FCV, whereas the other ISGs tested in this study failed. Further, we found that IRF1 was localized in the nucleus and efficiently activated IFN-β and the ISRE promoter. IRF1 can trigger the production of endogenous interferon and the expression of ISGs, suggesting that IRF1 can positively regulate IFN signalling. Importantly, the mRNA and protein levels of IRF1 were reduced upon FCV infection, which may be a new strategy for FCV to evade the innate immune system. Finally, the antiviral activity of IRF1 against feline panleukopenia virus, feline herpesvirus, and feline infectious peritonitis virus was demonstrated. These data indicate that feline IRF1 plays an important role in regulating the host type I IFN response and inhibiting feline viral infections.

Structure and regulation of the human interferon regulatory factor 1 (IRF-1) and IRF-2 genes: implications for a gene network in the interferon system

1994 ◽  
Vol 14 (2) ◽  
pp. 1500-1509
Author(s):  
H Harada ◽  
E Takahashi ◽  
S Itoh ◽  
K Harada ◽  
T A Hori ◽  
...  
Keyword(s):  
Gene Network ◽  
Interferon Regulatory Factor ◽  
Chromosomal Mapping ◽  
Human Interferon ◽  
Type I ◽  
Regulatory Factor ◽  
Nf Kappa B ◽  
Interferon Regulatory Factor 1 ◽  
Two Factors ◽  
Dna Binding Factors

Interferon regulatory factor 1 (IRF-1) and IRF-2 are structurally similar DNA-binding factors which were originally identified as regulators of the type I interferon (IFN) system; the former functions as a transcriptional activator, and the latter represses IRF-1 function by competing for the same cis elements. More recent studies have revealed new roles of the two factors in the regulation of cell growth; IRF-1 and IRF-2 manifest antioncogenic and oncogenic activities, respectively. In this study, we determined the structures and chromosomal locations of the human IRF-1 and IRF-2 genes and further characterized the promoters of the respective genes. Comparison of exon-intron organization of the two genes revealed a common evolutionary structure, notably within the exons encoding the N-terminal portions of the two factors. We confirmed the chromosomal mapping of the human IRF-1 gene to 5q31.1 and newly assigned the IRF-2 gene to 4q35.1, using fluorescence in situ hybridization. The 5' regulatory regions of both genes contain highly GC-rich sequences and consensus binding sequences for several known transcription factors, including NF-kappa B. Interestingly, one IRF binding site was found within the IRF-2 promoter, and expression of the IRF-2 gene was affected by both transient and stable IRF-1 expression. In addition, one potential IFN-gamma-activated sequence was found within the IRF-1 promoter. Thus, these results may shed light on the complex gene network involved in regulation of the IFN system.

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