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Fig. 3 | Stem Cell Research & Therapy

Fig. 3

From: Spotlight on therapeutic efficiency of mesenchymal stem cells in viral infections with a focus on COVID-19

Fig. 3

Possible immune system reactions in COVID-19 patients. To create an antiviral response, the innate immune system requires to diagnose the invasion of the viral, frequently via PAMPs. For the SARS-CoV-2, it is recognized that PAMPs in the shape of viral genomic RNA or the mediators in viral replication, such as dsRNA, are identified via either the endosomal RNA receptors, TLR3 and TLR7 and the cytosolic RNA sensor, and retinoic acid-inducible gene I/melanoma differentiation-associated gene 5 (RIG-I/MDA5). This detection occurrence triggers the downstream signaling cascade, including IRF3 and NF-κB, accompanied by their nuclear translocation. Type I IFN by interferon-α/β receptor (IFNAR), respectively, triggers the JAKs, STATs pathway, where JAK1 and tyrosine kinase 2 (TYK2) kinases phosphorylate STAT1 and STAT2. STAT1/2 organize a complex by IRF9, and simultaneously they transfer to the nucleus to initiate the transcription of IFN-stimulated genes (ISGs) with the regulation of IFN-stimulated response element (ISRE) comprising promoters [51]. Moreover, the SARS-CoV-2 is possible that trigger the inflammasome sensor, NACHT, LRR, and PYD domains-containing protein 3 (NALP3), leading to the release of the greatly inflammatory cytokine IL-1β and cause of pyroptosis, which is an inflammatory led to cell death. Envelope proteins and 3a-nsp of SARS caused the creation of the NLRP3 inflammasome [132, 133]

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