Epithelial antiviral response pathway

The epithelial antiviral response pathway represents the primary innate defense mechanism of mucosal surfaces, particularly in the respiratory, gastrointestinal, and urogenital tracts. This pathway is initiated by the recognition of pathogen-associated molecular patterns (PAMPs) by pattern recognition receptors (PRRs) such as Toll-like receptors (TLRs) and RIG-I-like receptors (RLRs) [1.1.3, 1.1.4]. Upon activation, these receptors trigger signaling cascades involving adaptor proteins like MAVS and STING, leading to the activation of IRF3 and IRF7 transcription factors and the subsequent production of Type I and Type III interferons (IFNs) [1.1.4]. Type III IFNs (IFN-lambda) are especially critical in epithelial cells as their receptors are primarily restricted to these tissues, providing a localized antiviral state without the systemic inflammation often associated with Type I IFNs [1.2.4]. Dysregulation of these pathways is linked to increased susceptibility to viral infections like influenza and COVID-19, as well as chronic inflammatory conditions like asthma and COPD [1.1.1, 1.2.4]. Therapeutic strategies include the use of IFN-lambda analogs, TLR agonists, and RIG-I activators to bolster the epithelial barrier and prevent viral spread [1.2.1, 1.2.4].

Other names

Epithelial innate immune responseMucosal antiviral responseType III interferon pathwayEpithelial innate immunity

Modulation of innate immune signaling through the activation of pattern recognition receptors (PRRs) or the administration of exogenous interferons to induce an antiviral state and the expression of interferon-stimulated genes (ISGs) in epithelial cells [1.1.3, 1.2.4].