Interferon

Interferons are cytokines named for their ability to interfere with viral replication. Type I comprises the interferon alpha subtypes and interferon beta, made by most cell types and signalling through a shared receptor. Type II is a single molecule, interferon gamma, made mainly by T and natural killer cells and acting on a separate receptor. Type III, the lambda interferons, act on a receptor largely confined to epithelium. All three converge on JAK-STAT signalling and induce hundreds of interferon-stimulated genes that block viral replication and raise MHC class I display.

Peginterferon alfa-2a, whose PEGylation extends the half-life enough for weekly dosing, was standard therapy for chronic hepatitis C until direct-acting antivirals displaced it. Interferon beta remains an approved disease-modifying treatment for relapsing multiple sclerosis, and interferon gamma-1b is approved for chronic granulomatous disease. The flu-like syndrome and cytopenias they cause are dose-related and mechanistic, not idiosyncratic.

Interferon activity is not a marker of a healthy immune system. A sustained type I signature is a defining abnormality in systemic lupus erythematosus, and anifrolumab, which blocks the type I receptor, is approved for that disease. Whether more interferon is desirable depends on which infection or autoimmune state is at issue.

The error worth naming is the claim that a compound boosts interferon, usually resting on raised interferon gamma in a stimulated whole-blood culture. That shows a cell responded, not that a person is protected; interferon-gamma release assays use the same readout to detect tuberculosis exposure, not immune strength. Listings describing research peptides as interferon inducers rarely say which of the three families they mean.