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Fig. 1 | Journal of Inflammation

Fig. 1

From: Cellular and molecular features of COVID-19 associated ARDS: therapeutic relevance

Fig. 1

IFNs signalling pathway activation mediated by intracellular TLRs following viral infection. Several intracellular TLRs such as TLR-3 and -7 can recognize viral RNA of SARS-CoV-2, activating several intracellular pro-inflammatory pathways including NF-κB and inducing transcription and release of several pro-inflammatory mediators (including IL-1β and IL-6) forming the so termed “cytokines storm”. Beetwen these mediators, also anti-viral cytokines such as IFNα, IFNβ, IFNγ can be released. The mediators IFNAR1, -2 and JAK1, -2, respectively can activate intracellular anti-inflammatory pathways involving STAT1, -2, mediating expression of ISGs. Abbreviations: GAS: interferon-gamma activated sequence; IFN: interferon; IFNAR: interferon-alpha, -beta, and -omega receptor; IRF: IFN regulatory factor; ISGs: interferon-stimulated gene; JAK: janus-kinase; MyD88: myeloid differentiation primary response gene 88; NF-κB: nuclear factor kappa B; P:phosphate; RNA: ribonucleic acid; STAT: signal transducer and activator of transcription; TLR: toll-like receptor; TRIF: TIR domain containing adapter inducing interferon β

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