Abstract
Healthy tissues of the body express relatively low basal levels of interferons. However, following detection of microbial invasion by sentinel receptors, a cascade of events initiates leading to the transcriptional induction of interferon genes. Interferons are secreted and act primarily as paracrine cytokines to bind neighboring cell surface receptors. Binding to interferon receptors activates a signal pathway to the nucleus inducing a set of interferon-stimulated genes. The biological activity of these genes confers the unique antiviral and innate immune response of interferons. The rapid induction of interferons is critical to survival, and equally critical is the recovery from this defensive state. Either an aberrant response to infection or an inherited genetic disorder that leads to sustained or increased interferon levels can tip the balance towards pathogenesis.
| Original language | English |
|---|---|
| Article number | 101282 |
| Journal | Seminars in Immunology |
| Volume | 43 |
| DOIs | |
| State | Published - Jun 2019 |
Keywords
- Autoinflammatory disease
- Inborn genetic mutations
- Type I interferonopathy
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