Vol. 3, Issue 6, Part A (2018)

Author(s): Haftay Abraha

Abstract: Interferon (INF) is one of the important cytokines groups, an essential component of the immune system. It is produced in response to microbes and other antigens that mediate and regulate immune and inflammatory reactions. They are classified into two types: type-I (IFN-α, β) and type-II (IFN-γ). Type-I IFNs consist of two distinct groups of proteins called IFN-α and IFN-β. Mononuclear phagocytes are the major source of IFN-α, whereas IFN-β is produced by many cells, such as fibroblasts. The most potent stimulus for type-I IFN synthesis is viral infection; antigen-activated T-cells also stimulate mononuclear phagocytes to synthesize type-I IFNs. The biological action of Type-I IFNs have been associated with antiviral immunity for several decades. More recently studies have been shown its role in non-viral infections, bacterial and protozoan infections. The several antiviral functions of the IFN-I include direct suppression of viral replication and activation of the immune response against viruses. In addition to their antiviral effects, IFN-I are also protective against several extracellular bacterial infections, in part, by promoting the induction of TNF-α and nitric oxide. Even though there is a subsequent loss of host resistance later in infection, type-I IFNs play a role in early resistance to protozoan parasites like trypanosome. In contrast, there is a negative effect of IFN-I on host resistance during chronic viral infection and acute infections with intracellular bacteria. Due to chronic IFN-I signaling induce adaptive immune system suppression and during acute intracellular bacterial infection, IFN-I suppress innate immunity respectively. Despite its limitations, interferons have been prepared in biotechnology industry for the treatment of diseases like hepatitis, sclerosis and cancer. Hence, further studies should be done to determine biological outcomes of IFN-I for many classes of bacterial, protozoa and other non-viral pathogens and also to determine the applicability of IFN-I modulation as a therapeutic to important chronic human viral infections.