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Interferon (IFN) is a class of cytokines produced by monocytes and lymphocytes. The main component of IFN is glycoprotein. IFN inhibits viral replication effectively through the action of cell-surface receptors that cause cells to produce antiviral proteins. Additionally, IFN enhances the vitality of natural killer cells (NK cells), macrophages, and T-lymphocytes, playing an immunomodulatory role. As a broad-spectrum antiviral agent, IFN can affect cell growth, differentiation, and modulation of immune function. It is currently one of the most important biologics for antiviral infection and antitumor treatment. IFNs are mainly classified into type I, type II, and type III. Type I has the most members of the IFN family, the type III family has four members, and the type II IFN family consists only of IFNγ, each of which has multiple important roles in the immune system.
Figure 1. Mechanisms of action and effects of type I interferons (IFNs) during infection with bacterial pathogens. (Kovarik P, et al., 2016)
IFN-I is a class of proteins involved in RNA and protein synthesis that are genetically regulated and have broad-spectrum antiviral activity. In humans, IFN-I includes IFN-α, IFN-β, IFN-κ, IFN-ω, and IFN-ε. Studies have shown that IFN-I has an anti-HIV effect and induces an antiviral immune response in the body, thereby inhibiting HIV replication and playing a role in the clearance of HIV reservoirs. Chronic immune activation caused by IFN-I may lead to immune failure and accelerate the progression of AIDS. Additionally, exogenous IFN, particularly IFN-α treatment, can induce systemic lupus erythematosus (SLE). Enhanced IFN signaling in peripheral blood mononuclear cells can be detected in 50%-80% of SLE patients, and the IFN-I level is associated with disease activity, relapse risk, and specific manifestations such as lupus nephritis (LN). Furthermore, autoimmune diseases, including rheumatoid arthritis, have been observed to exhibit heightened IFN-I responses. IFN-I also plays a crucial role in immune responses triggered by viral infections and kidney injury.
IFN-II consists only of IFN-γ and is important in coordinating innate and adaptive immune responses. In an inflammatory environment, IFN-γ activates the immune response, promotes pathogen elimination, and prevents excessive immune system activation and tissue damage. In the tumor microenvironment (TME), IFN-γ maintains a balance between pro- and anti-tumor immunity. IFN-γ inhibits angiogenesis, impairs endothelial cell proliferation and survival, and induces tumor mesenchymal ischemia. IFNγR is expressed on blood endothelial cells, and its involvement leads to vascular destruction and necrosis, which are important mechanisms for tumor rejection. IFN-γ upregulates IDO in melanoma cells and recruits Treg cells to avoid immune recognition, which supports tumorigenesis.
IFN-III comprises IFN-λ1, IFN-λ2, IFN-λ3, and IFN-λ4. Similar to IFN-I, IFN-λ mainly inhibits viral infections and has demonstrated anti-HBV efficacy in vitro. The biological effects of IFN-λs include antiviral activity, tumor antiproliferation, cytokine response modulation, and immune system regulation. Overexpression of IFN-λ has been found to inhibit the formation of subcutaneous and metastatic tumors. IFN-λ has potential applications in immune disorders, such as inflammatory bowel disease, that cause damage to the gastrointestinal epithelium.
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