Interferons

Polypeptides with antiviral, antiproliferative and immunomodulatory properties. A distinction is made between:

Type I interferons:

• INF-alfa (formerly known as leukocyte interferons)
• IFN-beta (fibroblast interferon)

Type II interferon:

• IFN-gamma (immune interferon)

The term type II interferon was introduced for IFN-gamma to distinguish it from the acid-stable type I interferons. Interferons were discovered due to their ability to interfere with viral replication. Later, the antiproliferative activity of interferons was additionally found. In addition, there is a further growing number of biological activities.

The type I interferons have a higher antiviral, the IFN-gamma a stronger antiproliferative effect. Interferons are used as effective drugs in various viral, immunological and oncological diseases. The immunoregulatory effects are more diverse for IFN-gamma than for type I interferons. All interferons induce MHC cell surface antigens and activate CD8+ T lymphocytes and natural killer cells (see also type I interferonopathies).

Type II interferons: IFN-gamma further induces MHCII antigens and activates macrophages.

Induction of IFN α-gene transcription and IFN β-gene transcription in virus-infected cells is an essential component of innate immunity. Virus-stimulated leukocytes produce mainly IFN-α. Fibroblasts produce mainly or even exclusively IFN-β. Although almost any cell type can produce IFN-alfa or IFN-beta after viral infection, there are cells that secrete up to a thousandfold amount of IFN.

These so-called "natural interferon-producing cells" also called NIPCs, are described as cells with a plasmacytoid morphology. Apparently, they play an important role in innate immune defense. Toll-like receptors are of particular importance in the recognition of pathogenic processes and subsequent type I IFN induction. Glucocorticoids and catecholamines, on the other hand, the major stress hormones, inhibit the synthesis of proinflammatory cytokines, such as interleukin-2, tumor necrosis factor-alfa, and IFN-gamma. This establishes a link to increased susceptibility to bacterial and viral infections during acute periods of stress.