Relevance of interleukin-10RB to chronic hepatitis B virus infection and biological activities of interferon-λ and interleukin-22

Cho, Okki; Cheong, Jae Youn; Jun, Ka Jung; Kim, Soon Sun; Chwae, Yong‐Joon; Kim, Kyongmin; Park, Sun; Cho, Sung Won

doi:10.1007/s12072-012-9361-8

Cited by 4 publications

(4 citation statements)

References 32 publications

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“…The HCA is a rapid viral molecular diagnostic method in which the specific single-stranded RNA probe is directly hybridized with denatured complementary DNA (cDNA) sequence as the target nucleic acid in a clinical sample. The HCA is used for detecting and identifying HBV and HCV ( Table 1 ) ( 5 , 35 , 39 ).…”

Section: Resultsmentioning

confidence: 99%

Nucleic Acid-Based Approaches for Detection of Viral Hepatitis

Behzadi

Ranjbar

Alavian

2014

Jundishapur J Microbiol

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Context:To determining suitable nucleic acid diagnostics for individual viral hepatitis agent, an extensive search using related keywords was done in major medical library and data were collected, categorized, and summarized in different sections.Results:Various types of molecular biology tools can be used to detect and quantify viral genomic elements and analyze the sequences. These molecular assays are proper technologies for rapidly detecting viral agents with high accuracy, high sensitivity, and high specificity. Nonetheless, the application of each diagnostic method is completely dependent on viral agent.Conclusions:Despite rapidity, automation, accuracy, cost-effectiveness, high sensitivity, and high specificity of molecular techniques, each type of molecular technology has its own advantages and disadvantages.

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Section: Resultsmentioning

confidence: 99%

Nucleic Acid-Based Approaches for Detection of Viral Hepatitis

Behzadi

Ranjbar

Alavian

2014

Jundishapur J Microbiol

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“…56 Cho's experimental results showed that IL10RB possibly caused chronic hepatitis B because cytokines combined with IL10RB can affect hepatocellular disease by regulating immune cells. 57 IFNL3 influences the severity of liver inflammation and fibrosis in viral and nonviral liver diseases. 58 In Figure 4F, those HBCD targets with d s = 1 in the overlap network, such as AR, MAPK1, and MAPK14, could regulate CEBPB to affect IL10, then IL10RB and IFNL3 could be mediated by IL10.…”

Section: Discussionmentioning

confidence: 99%

“…The inflammatory cytokine IL10RB could lead to liver fibrosis while it is differentially expressed in the nonalcoholic steatohepatitis adipose tissue . Cho’s experimental results showed that IL10RB possibly caused chronic hepatitis B because cytokines combined with IL10RB can affect hepatocellular disease by regulating immune cells . IFNL3 influences the severity of liver inflammation and fibrosis in viral and nonviral liver diseases .…”

Section: Discussionmentioning

confidence: 99%

Probing the Mechanism of Hepatotoxicity of Hexabromocyclododecanes through Toxicological Network Analysis

Dai

Tang

Dai

et al. 2020

Environ. Sci. Technol.

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The prediction and mechanism analysis of hepatotoxicity of contaminants, because of their various phenotypes and complex mechanisms, is still a key problem in environmental research. We applied a toxicological network analysis method to predict the hepatotoxicity of three hexabromocyclododecane (HBCD) diastereoisomers (α-HBCD, β-HBCD, and γ-HBCD) and explore their potential mechanisms. First, we collected the hepatotoxicity related genes and found that those genes were significantly localized in the human interactome. Therefore, these genes form a disease module of hepatotoxicity. We also collected targets of α-, β-, and γ-HBCD and found that their targets overlap with the hepatotoxicity disease module. Then, we trained a model to predict hepatotoxicity of three HBCD diastereoisomers based on the relationship between the hepatotoxicity disease module and targets of compounds. We found that 593 genes were significantly located in the hepatotoxicity disease module (Z = 11.9, p < 0.001) involved in oxidative stress, cellular immunity, and proliferation, and the accuracy of hepatotoxicity prediction of HBCD was 0.7095 ± 0.0193 and the recall score was 0.8355 ± 0.0352. HBCD mainly affects the core disease module genes to mediate the adenosine monophosphate-activated kinase, p38MAPK, PI3K/Akt, and TNFα pathways to regulate the immune reaction and inflammation. HBCD also induces the secretion of IL6 and STAT3 to lead hepatotoxicity by regulating NR3C1. This approach is transferable to other toxicity research studies of environmental pollutants.

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“…IFN-α, which is expressed during viral infections, upregulates IL-22α on keratinocytes. In this context, IL-22 inhibits the differentiation of keratinocytes and increases the thickness of the epidermis, thereby mediating innate immune defense against viral infection [ 30 , 31 ]. In addition, the expression of IL-22Rα is significantly increased in the epidermis of patients with psoriasis [ 32 , 33 ].…”

Section: Introductionmentioning

confidence: 99%

The pathogenic role of interleukin-22 and its receptor during UVB-induced skin inflammation

et al. 2017

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Recent studies show that IL-22, a cytokine produced by activated CD4+ T cells and NK cells, plays a pathogenic role in acute and chronic skin diseases. While IL-22 is produced by immune cells, the expression of IL-22Rα, the functional subunit of IL-22R, is mostly restricted to non-hematopoietic cells in organs such as the skin and pancreas. Although it is well known that ultraviolet B (UVB) radiation induces skin inflammation, there have been no reports regarding the effect of UVB on the expression of IL-22Rα. This study investigated IL-22Rα expression and IL-22-mediated proliferation and pro-inflammatory cytokine production by UVB-irradiated keratinocytes. IL-22Rα was increased in HaCaT and primary human keratinocytes after UVB irradiation through the translocation of IL-22Rα from the cytosol to the membrane. This increase in the expression of IL-22Rα was mediated by the PI3K/Akt pathway. Moreover, the suppression of keratinocyte proliferation by UVB irradiation was inhibited by treatment with IL-22. At the same time, IL-22 increased the production of IL-1α, IL-6, and IL-18 in UVB-irradiated HaCaT cells and primary human keratinocytes. Finally, IL-22Rα expression was increased in UVB-irradiated human and mouse skin by immunohistochemistry. The increased expression of IL-22Rα therefore promotes keratinocyte proliferation and pro-inflammatory cytokine production during UVB-induced skin inflammation, suggesting that UVB facilitates skin inflammation by increasing the responsiveness of keratinocytes to IL-22. This study provides a new insight into UVB-induced skin inflammation and the regulation of related inflammatory skin diseases.

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Relevance of interleukin-10RB to chronic hepatitis B virus infection and biological activities of interferon-λ and interleukin-22

Cited by 4 publications

References 32 publications

Nucleic Acid-Based Approaches for Detection of Viral Hepatitis

Nucleic Acid-Based Approaches for Detection of Viral Hepatitis

Probing the Mechanism of Hepatotoxicity of Hexabromocyclododecanes through Toxicological Network Analysis

The pathogenic role of interleukin-22 and its receptor during UVB-induced skin inflammation

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