Editing Interferon (section)

== Function ==
All interferons share several common effects: they are antiviral agents and they modulate functions of the immune system.  Administration of Type I IFN 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 infect nearby cells. However, the infected cell can protect neighboring cells against a potential infection of the virus by releasing interferons.  In response to interferon, cells produce large amounts of an [[enzyme]] known as [[protein kinase R]] (PKR). This enzyme [[phosphorylation|phosphorylates]] a protein known as [[eIF-2]] in response to new viral infections; 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 interferon 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 infected host cells. In addition, interferons induce production of hundreds of other proteins—known collectively as interferon-stimulated genes (ISGs)—that have roles in combating viruses and other actions produced by interferon.<ref>{{cite journal | vauthors = Fensterl V, Sen GC | title = Interferons and viral infections | journal = BioFactors | volume = 35 | issue = 1 | pages = 14–20 | year = 2009 | pmid = 19319841 | doi = 10.1002/biof.6 | s2cid = 27209861 }}</ref><ref>{{cite journal | vauthors = de Veer MJ, Holko M, Frevel M, Walker E, Der S, Paranjape JM, Silverman RH, Williams BR | title = Functional classification of interferon-stimulated genes identified using microarrays | journal = Journal of Leukocyte Biology | volume = 69 | issue = 6 | pages = 912–920 | date = June 2001 | pmid = 11404376 | doi = 10.1189/jlb.69.6.912 | s2cid = 1714991 | doi-access = free }}</ref>
They also limit viral spread by increasing [[p53]] activity, which kills virus-infected cells by promoting [[apoptosis]].<ref name="Takaoka">{{cite journal | vauthors = Takaoka A, Hayakawa S, Yanai H, Stoiber D, Negishi H, Kikuchi H, Sasaki S, Imai K, Shibue T, Honda K, Taniguchi T | title = Integration of interferon-alpha/beta signalling to p53 responses in tumour suppression and antiviral defence | journal = Nature | volume = 424 | issue = 6948 | pages = 516–523 | date = July 2003 | pmid = 12872134 | doi = 10.1038/nature01850 | doi-access = free | bibcode = 2003Natur.424..516T }}</ref><ref>{{cite journal | vauthors = Moiseeva O, Mallette FA, Mukhopadhyay UK, Moores A, Ferbeyre G | title = DNA damage signaling and p53-dependent senescence after prolonged beta-interferon stimulation | journal = Molecular Biology of the Cell | volume = 17 | issue = 4 | pages = 1583–1592 | date = April 2006 | pmid = 16436515 | pmc = 1415317 | doi = 10.1091/mbc.E05-09-0858 }}</ref>  The effect of IFN on p53 is also linked to its protective role against certain cancers.<ref name="Takaoka" />

Another function of interferons is to up-regulate [[major histocompatibility complex]] molecules, [[MHC I]] and [[MHC II]], and increase  [[immunoproteasome]] activity. All interferons significantly enhance the presentation of MHC I dependent antigens. [[Interferon gamma|Interferon gamma (IFN-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 cell]]s, while the immunoproteasome processes these peptides for loading onto the MHC I molecule, thereby increasing the recognition and killing of infected or malignant cells.  Higher MHC II expression increases presentation of these peptides to [[helper T cell]]s; these cells release cytokines (such as more interferons and [[interleukins]], among others) that signal to and co-ordinate the activity of other immune cells.<ref name=":0">{{cite journal | vauthors = Ikeda H, Old LJ, Schreiber RD | title = The roles of IFN gamma in protection against tumor development and cancer immunoediting | journal = Cytokine & Growth Factor Reviews | volume = 13 | issue = 2 | pages = 95–109 | date = April 2002 | pmid = 11900986 | doi = 10.1016/s1359-6101(01)00038-7 }}</ref><ref name=":1">{{cite journal | vauthors = Dunn GP, Bruce AT, Sheehan KC, Shankaran V, Uppaluri R, Bui JD, Diamond MS, Koebel CM, Arthur C, White JM, Schreiber RD | title = A critical function for type I interferons in cancer immunoediting | journal = Nature Immunology | volume = 6 | issue = 7 | pages = 722–729 | date = July 2005 | pmid = 15951814 | doi = 10.1038/ni1213 | s2cid = 20374688 }}</ref><ref name=":2">{{cite journal | vauthors = Borden EC, Sen GC, Uze G, Silverman RH, Ransohoff RM, Foster GR, Stark GR | title = Interferons at age 50: past, current and future impact on biomedicine | journal = Nature Reviews. Drug Discovery | volume = 6 | issue = 12 | pages = 975–990 | date = December 2007 | pmid = 18049472 | pmc = 7097588 | doi = 10.1038/nrd2422 }}</ref>

Interferons can also suppress [[angiogenesis]] by down regulation of [[Angiogenesis|angiogenic]] stimuli deriving from tumor cells. They also suppress the proliferation of [[Endothelium|endothelial]] cells. Such suppression causes a decrease in tumor angiogenesis, a decrease in its [[Angiogenesis|vascularization]] and subsequent growth inhibition. Interferons, such as [[interferon gamma]], directly activate other immune cells, such as [[macrophage]]s and [[natural killer cell]]s.<ref name=":0" /><ref name=":1" /><ref name=":2" />