Host immune pathways and interferon signaling (IFN signaling)

Host immune pathways and interferon signaling represent a complex network of cellular processes designed to detect and eliminate pathogens, particularly viruses. Upon recognition of pathogen-associated molecular patterns (PAMPs) by pattern recognition receptors (PRRs), cells produce interferons, which are pleiotropic cytokines categorized into Types I, II, and III (PubMed: 28231293). These interferons bind to specific cell-surface receptors, such as the Type I interferon receptor (IFNAR), triggering the Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway (UniProt: P17181). This signaling cascade leads to the transcription of hundreds of interferon-stimulated genes (ISGs) that establish an antiviral state, inhibit viral replication, and modulate the adaptive immune response (PubMed: 25251363). Dysregulation of these pathways is central to various pathologies; overactivation can lead to systemic lupus erythematosus (SLE) or interferonopathies, while impaired signaling can result in severe viral susceptibility or cancer progression (PubMed: 30546106). Therapeutic strategies include the administration of recombinant interferons for viral hepatitis or multiple sclerosis, and the use of JAK inhibitors or monoclonal antibodies against IFN receptors to treat autoimmune conditions (PubMed: 32103181). Because this entry describes a broad biological system rather than a single protein, it is classified as a pathway rather than a discrete therapeutic target.

Other names

Innate immune responseType I interferon signalingJAK-STAT pathwayAntiviral responseInterferon signaling pathway

Drugs targeting this pathway function as either agonists that mimic endogenous interferons to induce antiviral and antiproliferative states, or as antagonists (e.g., monoclonal antibodies or JAK inhibitors) that block signaling to alleviate autoimmune inflammation (PubMed: 32103181).