All<unk> s share several common effects: they are antiviral agents and they modulate functions of the immune system. Administration of Type I<unk>  has been shown experimentally to inhibit tumor growth in animals, but the beneficial action in human tumors has not been widely documented. A virus-infected cell releases viral particles that can<unk> ect nearby cells. However, the<unk> ected cell can protect neighboring cells against a potential<unk> ection of the virus by releasing<unk> s. In response to<unk> , cells produce large amounts of an enzyme known as protein kinase R (PKR). This enzyme phosphorylates a protein known as eIF-2 in response to new viral<unk> ections; the phosphorylated eIF-2 forms an inactive complex with another protein, called eIF2B, to reduce protein synthesis within the cell. Another cellular enzyme, RNAse L—also induced by<unk>  action—destroys RNA within the cells to further reduce protein synthesis of both viral and host genes. Inhibited protein synthesis impairs both virus replication and<unk> ected host cells. In addition,<unk> s induce production of hundreds of other proteins—known collectively as<unk> -stimulated genes (ISGs)—that have roles in combating viruses and other actions produced by<unk> . They also limit viral spread by increasing p53 activity, which kills virus-infected cells by promoting apoptosis. The effect of<unk>  on p53 is also linked to its protective role against certain cancers. Another function of<unk> s is to up-regulate major histocompatibility complex molecules, MHC I and MHC II, and increase immunoproteasome activity. All<unk> s significantly enhance the presentation of MHC I dependent antigens.<unk>  gamma <unk> -gamma) also significantly stimulates the MHC II-dependent presentation of antigens. Higher MHC I expression increases presentation of viral and abnormal peptides from cancer cells to cytotoxic T cells, while the immunoproteasome processes these peptides for loading onto the MHC I molecule, thereby increasing the recognition and killing of<unk> ected or malignant cells. Higher MHC II expression increases presentation of these peptides to helper T cells; these cells release cytokines (such as more<unk> s and interleukins, among others) that signal to and co-ordinate the activity of other immune cells.<unk> s can also suppress angiogenesis by down regulation of angiogenic stimuli deriving from tumor cells. They also suppress the proliferation of endothelial cells. Such suppression causes a decrease in tumor angiogenesis, a decrease in its vascularization and subsequent growth inhibition.<unk> s, such as<unk>  gamma, directly activate other immune cells, such as macrophages and natural killer cells.
Interferon
Pegylated interferon
Peginterferon alfa-2a
Peginterferon alfa-2b
Ropeginterferon alfa-2b
Peginterferon beta-1a
Ruxolitinib
Rituximab