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10.2147/JIR.S301476

http://scihub22266oqcxt.onion/10.2147/JIR.S301476
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33833547!8021260!33833547
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suck abstract from ncbi


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pmid33833547      J+Inflamm+Res 2021 ; 14 (ä): 1257-1270
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  • Interferon-lambda3 Exacerbates the Inflammatory Response to Microbial Ligands: Implications for SARS-CoV-2 Pathogenesis #MMPMID33833547
  • Read SA; Gloss BS; Liddle C; George J; Ahlenstiel G
  • J Inflamm Res 2021[]; 14 (ä): 1257-1270 PMID33833547show ga
  • INTRODUCTION: Interferon lambdas (IFN-lambdas) are antiviral cytokines that restrict pathogen infection and dissemination at barrier surfaces. Controlled expression of IFN-lambdas efficiently eliminates acute infections by activating a suite of interferon stimulated genes that inhibit viral propagation and activate local immune cells. Excessive or prolonged production of IFN-lambdas can however mediate tissue inflammation and disrupt epithelial barriers in both viral and non-viral disease. The mechanism by which IFN-lambdas drive this disease pathogenesis is poorly understood but may be caused by IFN-lambda-mediated amplification of other innate immune signaling pathways. METHODS: Monocyte-derived macrophages were differentiated +/- IFN-lambda3 and treated with KDO-lipid A, poly I:C or zymosan, representing bacterial, viral or fungal ligands, respectively. Transcriptome and protein expression were quantified by RNA sequencing/PCR and ELISA/bead array, respectively. Bioinformatic analysis was used to define transcription factor profiles and signaling pathways amplified by IFN-lambda3. Finally, the SARS-CoV-2 dataset GSE152075 was queried to compare the effects of IFNL versus IFNA expression in relation to viral load and nasopharyngeal transcriptomes. RESULTS: IFN-lambda3 exacerbated inflammatory and chemotactic responses unique to each microbial ligand, as measured by RNA sequencing and by ELISA/bead array. Functional annotation identified pathways amplified by IFN-lambda3, including inflammasome activation. Inflammasome amplification was confirmed in vitro, as measured by caspase 1 activity and IL-1beta cleavage. Lastly, SARS-CoV-2 infected nasopharyngeal transcriptomes expressing IFN-lambdas but not IFN-alphas were implicated in myeloid cell-driven pathogenesis including neutrophil degranulation, complement and coagulation cascades. DISCUSSION: These data suggest that IFN-lambdas contribute to disease pathology by exacerbating innate immune responses during chronic or severe disease states. IFN-lambdas may contribute to SARS-CoV-2 disease severity, however further study is required to confirm true causation.
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