Transcription Factor MafB Suppresses Type I Interferon Production by CD14+ Monocytes in Patients With Chronic Hepatitis C

Liu, Tiemei; Wang, Han; Zhang, Dongna; Zhu, Guangyu

doi:10.3389/fmicb.2019.01814

Cited by 11 publications

(10 citation statements)

References 33 publications

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“…MAFB promotes an anti-inflammatory function in inflamed lungs leading to M2 macrophage polarization ( 78 , 79 ). Interestingly, the expression of MAFB in macrophages is associated with an impaired type I interferon response in chronic hepatitis virus ( 80 ). Finally, CCL2 and CXCL10 genes lacked expression in moderate patients; only CXCL10 had higher expression in moderate M2 macrophages.…”

Section: Resultsmentioning

confidence: 99%

On Deep Landscape Exploration of COVID-19 Patients Cells and Severity Markers

et al. 2021

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COVID-19 is a disease with a spectrum of clinical responses ranging from moderate to critical. To study and control its effects, a large number of researchers are focused on two substantial aims. On the one hand, the discovery of diverse biomarkers to classify and potentially anticipate the disease severity of patients. These biomarkers could serve as a medical criterion to prioritize attention to those patients with higher prone to severe responses. On the other hand, understanding how the immune system orchestrates its responses in this spectrum of disease severities is a fundamental issue required to design new and optimized therapeutic strategies. In this work, using single-cell RNAseq of bronchoalveolar lavage fluid of nine patients with COVID-19 and three healthy controls, we contribute to both aspects. First, we presented computational supervised machine-learning models with high accuracy in classifying the disease severity (moderate and severe) in patients with COVID-19 starting from single-cell data from bronchoalveolar lavage fluid. Second, we identified regulatory mechanisms from the heterogeneous cell populations in the lungs microenvironment that correlated with different clinical responses. Given the results, patients with moderate COVID-19 symptoms showed an activation/inactivation profile for their analyzed cells leading to a sequential and innocuous immune response. In comparison, severe patients might be promoting cytotoxic and pro-inflammatory responses in a systemic fashion involving epithelial and immune cells without the possibility to develop viral clearance and immune memory. Consequently, we present an in-depth landscape analysis of how transcriptional factors and pathways from these heterogeneous populations can regulate their expression to promote or restrain an effective immune response directly linked to the patients prognosis.

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Section: Resultsmentioning

confidence: 99%

On Deep Landscape Exploration of COVID-19 Patients Cells and Severity Markers

et al. 2021

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“…For example, CEACAM1 is a receptor of murine hepatitis virus [ 65 ] and several bacteria; also the oligomerization of CEACAM1 mediate immune envision by inhibiting NK and T cell activity [ 66 ]. Mafb suppresses production of type I IFN by CD14+ monocytes, impairing antiviral responses [ 67 ]. Therefore, the miR-466i-5p activity was restricted by novel_circ_015884, novel_circ_016323 or novel_circ_024780, resulting in the increased level of target mRNAs such as CEACAM1 or Mafb and then perhaps contribute to the immune escape response of RABV.…”

Section: Discussionmentioning

confidence: 99%

Expression Profiling and Bioinformatics Analysis of CircRNA in Mice Brain Infected with Rabies Virus

Zhao

Wang

et al. 2021

IJMS

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Rabies virus (RABV) induces acute, fatal encephalitis in mammals including humans. The circRNAs are important in virus infection process, but whether circRNAs regulated RABV infection remains largely unknown. Here, mice brain with or without the RABV CVS-11 strain were subjected to RNA sequencing and a total of 30,985 circRNAs were obtained. Among these, 9021 candidates were shared in both groups, and 14,610 and 7354 circRNAs were expressed specifically to the control and experimental groups, indicating that certain circRNAs were specifically inhibited or induced on RABV infection. The circRNAs mainly derived from coding exons. In total, 636 circRNAs were differentially expressed in RABV infection, of which 426 significantly upregulated and 210 significantly downregulated (p < 0.05 and fold change ≥2). The expression of randomly selected 6 upregulated and 6 downregulated circRNAs was tested by RT-qPCR, and the expression trend of the 11 out of 12 circRNAs was consistent in RT- qPCR and RNA-seq analysis. Rnase R-resistant assay and Sanger sequencing were conducted to verify the circularity of circRNAs. GO analysis demonstrated that source genes of all differentially regulated circRNAs were mainly related to cell plasticity and synapse function. Both KEGG and GSEA analysis revealed that these source genes were engaged in the cGMP–PKG and MAPK signaling pathway, and HTLV-I infection. Also, pathways related to glucose metabolism and synaptic functions were enriched in KEGG analysis. The circRNA–miRNA–mRNA network was built with 25 of 636 differentially expressed circRNAs, 264 mRNAs involved in RABV infection, and 29 miRNAs. Several miRNAs and many mRNAs in the network were reported to be related to viral infection and the immune response, suggesting that circRNAs could regulate RABV infection via interacting with miRNAs and mRNAs. Taken together, this study first characterized the transcriptomic pattern of circRNAs, and signaling pathways and function that circRNAs are involved in, which may indicate directions for further research to understand mechanisms of RABV pathogenesis.

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“…Indeed, silencing of MAF expression in macrophages leads to macrophage re-programming toward an M1-like phenotype and enhancement of antitumor activities (19,20). In addition, MAFB has the ability of negatively regulating the expression of type I IFN upon viral infection by setting a threshold for IRF3-dependent transcription (21,22). Specifically, MAFB antagonizes antiviral responses as it blocks the recruitment of coactivators to the transcription factor IRF3 (22), and suppresses the monocyte production of type I IFN in chronic hepatitis C patients (21).…”

Section: Mafb and Maf Transcription Factors In Macrophagesmentioning

confidence: 99%

“…In addition, MAFB has the ability of negatively regulating the expression of type I IFN upon viral infection by setting a threshold for IRF3-dependent transcription (21,22). Specifically, MAFB antagonizes antiviral responses as it blocks the recruitment of coactivators to the transcription factor IRF3 (22), and suppresses the monocyte production of type I IFN in chronic hepatitis C patients (21). This function as "rheostat" for type I IFN (23) suggests that MAFB might contribute to the defective IFN production in COVID-19.…”

Section: Mafb and Maf Transcription Factors In Macrophagesmentioning

confidence: 99%