Editing Interferon beta-1a (section)

==Mechanism of action==
Interferon beta balances the expression of pro- and anti-inflammatory agents in the brain, and reduces the number of inflammatory cells that cross the [[blood brain barrier]].<ref name="pmid21649449">{{cite journal | vauthors = Kieseier BC | title = The mechanism of action of interferon-β in relapsing multiple sclerosis | journal = CNS Drugs | volume = 25 | issue = 6 | pages = 491–502 | date = June 2011 | pmid = 21649449 | doi = 10.2165/11591110-000000000-00000 | s2cid = 25516515 }}</ref> Overall, therapy with interferon beta leads to a reduction of neuron inflammation.<ref name="pmid21649449"/> Moreover, it is also thought to increase the production of [[nerve growth factor]] and consequently improve neuronal survival.<ref name="pmid21649449"/> In vitro, interferon beta reduces production of [[T helper 17 cell|Th17 cells]] which are a subset of T lymphocytes believed to have a role in the pathophysiology of MS.<ref>{{cite journal | vauthors = Mitsdoerffer M, Kuchroo V | title = New pieces in the puzzle: how does interferon-beta really work in multiple sclerosis? | journal = Annals of Neurology | volume = 65 | issue = 5 | pages = 487–488 | date = May 2009 | pmid = 19479722 | doi = 10.1002/ana.21722 | s2cid = 42050086 }}</ref>

[[File:Signal transduction pathways.svg|alt=A scalable vector graphic of signal transduction pathways|thumb|Cytokines, such as '''interferons''', typically activate second messenger systems, like JAK-STAT pathways, as illustrated on the left side of the diagram. Conversely, '''hormones''' typically activate different signaling pathways, like G protein-coupled receptors, seen at the top of the figure.]]