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Interferon beta (IFN-β) is a type I interferon cytokine produced primarily by fibroblasts and epithelial cells in response to viral and bacterial infections. It plays a central role in the innate immune response, serving as an early warning signal that induces antiviral defenses, modulates immune cell activities, and links innate and adaptive immunity. IFN-β and all type I interferons signal through the interferon alpha/beta receptor (IFNAR), which consists of two chains, IFNAR1 and IFNAR2. Ligand binding activates the JAK-STAT pathway, resulting in the transcription of hundreds of ISGs that block viral replication, induce apoptosis of infected cells, regulate inflammation, and promote immune resolution. IFN-β is used clinically to treat relapsing forms of multiple sclerosis, exploiting its immunomodulatory and anti-inflammatory properties. Safety concerns include flu-like symptoms, increased risk of depression, autoimmune exacerbation, and rare liver toxicity. Recent research highlights its role in inflammation resolution as well as classic antiviral defenses.
Interferon beta binds to the type I interferon receptor (IFNAR1 and IFNAR2). This binding activates the JAK-STAT pathway, which in turn induces the transcription of interferon-stimulated genes (ISGs) leading to an antiviral state. It also activates additional signaling cascades such as PI3K, MAPK p38, and CRKL. Furthermore, it inhibits viral protein synthesis (e.g., via eIF2a inactivation, RNase L activation), promotes anti-proliferative effects and cell death in infected or inflammatory cells, and modulates immune cell phenotypes and cytokine production.
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