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. 2021 Nov 10;12:731807. doi: 10.3389/fimmu.2021.731807

Figure 1.

Figure 1

(A) Graphical illustration of the induction of type III interferon gene expression upon rhinovirus infection. HRV enters the cell via ICAM-1 receptor, CDHR3 receptor or via clathrin-mediated LDLR endocytosis. Viral cytosolic and endosomal ssRNA and dsRNA can be detected by PRR and PRM such as RIG-1 or MDA-5 (cytosolic) or TLR3 and TLR7/8 (endosomal), respectively. PRR and PRM induce downstream signaling cascades leading to recruitment of IRFs and NF-κB that promote type III interferon gene expression in the nucleus. (B) Graphical illustration of the signaling pathway after TLR 7 and 8 activation by resiquimod (R848). TLR 7 and 8 are located in intracellular vesicles, where they bind ssRNA or substances that mimic their structure. After activation, the signal is transduced via Myeloid differentiation primary response 88 (MyD88). Important mediators are TNF receptor-associated factor (TRAF) 3 and 6 as well as different interleukin-1 receptor associated kinase family members (IRAKs). Interferon regulatory factors (IRF) 3 and 7 and nuclear factor ‘kappa-light-chain-enhancer’ of activated B-cells (NF-κB) are the key regulatory factors that influence the gene expression in the nucleus. As a result the production of pro-inflammatory cytokines and type I interferons is enhanced.