Editing Interferon (section)

==Types of interferon==
Based on the type of [[Immune receptor|receptor]] through which they signal, human interferons have been classified into three major types.
* [[Interferon type I]]: All type I IFNs bind to a specific cell surface receptor complex known as the IFN-α/β receptor ([[Interferon-alpha/beta receptor|IFNAR]]) that consists of [[IFNAR1]] and [[IFNAR2]] chains.<ref>{{cite journal | vauthors = de Weerd NA, Samarajiwa SA, Hertzog PJ | title = Type I interferon receptors: biochemistry and biological functions | journal = The Journal of Biological Chemistry | volume = 282 | issue = 28 | pages = 20053–20057 | date = July 2007 | pmid = 17502368 | doi = 10.1074/jbc.R700006200 | doi-access = free }}</ref>  The type I interferons present in humans are [[IFN-α]], [[IFN-β]], IFN-ε, [[IFNK|IFN-κ]] and [[Interferon type I#IFN-ω|IFN-ω]].<ref name=Liu>{{cite journal | vauthors = Liu YJ | title = IPC: professional type 1 interferon-producing cells and plasmacytoid dendritic cell precursors | journal = Annual Review of Immunology | volume = 23 | pages = 275–306 | date = 2005 | pmid = 15771572 | doi = 10.1146/annurev.immunol.23.021704.115633 }}</ref> Interferon beta ([[IFN-β]]) can be produced by all nucleated cells when they recognize that a virus has invaded them. The most prolific producers of IFN-α and IFN-β are [[plasmacytoid dendritic cell]]s circulating in the blood. [[Monocytes]] and [[macrophages]] can also produce large amounts of type I interferons when stimulated by viral molecular patterns. The production of type I IFN-α is inhibited by another cytokine known as Interleukin-10. Once released, type I interferons bind to the [[Interferon-alpha/beta receptor|IFN-α/β receptor]] on target cells, which leads to expression of proteins that will prevent the virus from producing and replicating its RNA and DNA.<ref>{{cite journal | vauthors = Levy DE, Marié IJ, Durbin JE | title = Induction and function of type I and III interferon in response to viral infection | journal = Current Opinion in Virology | volume = 1 | issue = 6 | pages = 476–486 | date = December 2011 | pmid = 22323926 | pmc = 3272644 | doi = 10.1016/j.coviro.2011.11.001 }}</ref> Overall, IFN-α can be used to treat hepatitis B and C infections, while IFN-β can be used to treat multiple sclerosis.<ref name="Cohen and Parkin" />
* [[Interferon type II]] ([[IFN-γ]] in humans): This is also known as immune interferon and is activated by Interleukin-12.<ref name="Cohen and Parkin" /> Type II interferons are also released by [[cytotoxic T cell]]s and type-1 [[T helper cell]]s. However, they block the proliferation of type-2 T helper cells. The previous results in an inhibition of [[Th2|T<sub>h</sub>2]] immune response and a further induction of [[Th1 cell|T<sub>h</sub>1]] immune response.<ref name=Kidd>{{cite journal | vauthors = Kidd P | title = Th1/Th2 balance: the hypothesis, its limitations, and implications for health and disease | journal = Alternative Medicine Review | volume = 8 | issue = 3 | pages = 223–246 | date = August 2003 | pmid = 12946237 }}</ref> IFN type II binds to [[IFNGR]], which consists of [[IFNGR1]] and [[IFNGR2]] chains.<ref name="Cohen and Parkin" />
* [[Interferon type III]]: Signal through a receptor complex consisting of [[Interleukin 10 receptor, beta subunit|IL10R2]] (also called CRF2-4) and [[IFNLR1]] (also called CRF2-12). Although discovered more recently than type I and type II IFNs,<ref>{{cite journal | vauthors = Kalliolias GD, Ivashkiv LB | title = Overview of the biology of type I interferons | journal = Arthritis Research & Therapy | volume = 12 | issue = Suppl 1 | pages = S1 | date = 2010 | pmid = 20392288 | pmc = 2991774 | doi = 10.1186/ar2881 | doi-access = free }}</ref> recent information demonstrates the importance of Type III IFNs in some types of virus or fungal infections.<ref>Vilcek, Novel interferons, Nature Immunol. 4, 8-9. 2003</ref><ref name="Hermant_2014">{{cite journal | vauthors = Hermant P, Michiels T | title = Interferon-λ in the context of viral infections: production, response and therapeutic implications | journal = Journal of Innate Immunity | volume = 6 | issue = 5 | pages = 563–574 | date = 2014 | pmid = 24751921 | pmc = 6741612 | doi = 10.1159/000360084 }}</ref><ref>{{cite journal | vauthors = Espinosa V, Dutta O, McElrath C, Du P, Chang YJ, Cicciarelli B, Pitler A, Whitehead I, Obar JJ, Durbin JE, Kotenko SV, Rivera A | title = Type III interferon is a critical regulator of innate antifungal immunity | journal = Science Immunology | volume = 2 | issue = 16 | pages = eaan5357 | date = October 2017 | pmid = 28986419 | pmc = 5880030 | doi = 10.1126/sciimmunol.aan5357 }}</ref>

In general, type I and II interferons are responsible for regulating and activating the immune response.<ref name="Cohen and Parkin" /> Expression of type I and III IFNs can be induced in virtually all cell types upon recognition of viral components, especially nucleic acids, by cytoplasmic and endosomal receptors, whereas type II interferon is induced by cytokines such as IL-12, and its expression is restricted to immune cells such as [[T cells]] and [[NK cells]].<ref>{{Cite journal |last1=Levy |first1=David E |last2=Marié |first2=Isabelle J |last3=Durbin |first3=Joan E |date=2011 |title=Induction and function of type I and III interferon in response to viral infection |journal=Current Opinion in Virology |language=en |volume=1 |issue=6 |pages=476–486 |doi=10.1016/j.coviro.2011.11.001 |pmid=22323926 |pmc=3272644 |issn=1879-6257 }}</ref>