Editing Complement system (section)

== Regulation ==
The complement system has the potential to be extremely damaging to host tissues, meaning its activation must be tightly regulated. The complement system is regulated by [[complement control protein]]s, which are present at blood plasma and host cell membrane.<ref>{{Cite journal |vauthors=Zewde N, Gorham RD, Dorado A, Morikis D |date=2016-03-31 |title=Quantitative Modeling of the Alternative Pathway of the Complement System |journal=PLOS ONE |volume=11 |issue=3 |pages=e0152337 |bibcode=2016PLoSO..1152337Z |doi=10.1371/journal.pone.0152337 |pmc=4816337 |pmid=27031863 |doi-access=free}}</ref> Some complement control proteins are present on the membranes of self-cells preventing them from being targeted by complement. One example is [[CD59]], also known as protectin, which inhibits C9 polymerization during the formation of the [[membrane attack complex]]. The classical pathway is inhibited by [[C1-inhibitor]], which binds to C1 to prevent its activation.<ref name=":2">{{Cite journal |vauthors=Bajic G, Degn SE, Thiel S, Andersen GR |date=November 2015 |title=Complement activation, regulation, and molecular basis for complement-related diseases |journal=The EMBO Journal |volume=34 |issue=22 |pages=2735–2757 |doi=10.15252/embj.201591881 |pmc=4682646 |pmid=26489954}}</ref>  Another example, is a plasma protein called, [[Factor H]] (FH), which has a key role in down-regulating the alternative pathway.<ref>{{Cite journal |display-authors=6 |vauthors=Zhang Y, Ghiringhelli Borsa N, Shao D, Dopler A, Jones MB, Meyer NC, Pitcher GR, Taylor AO, Nester CM, Schmidt CQ, Smith RJ |date=2020-12-15 |title=Factor H Autoantibodies and Complement-Mediated Diseases |journal=Frontiers in Immunology |volume=11 |pages=607211 |doi=10.3389/fimmu.2020.607211 |pmc=7770156 |pmid=33384694 |doi-access=free}}</ref>  Factor H, along with another protein called [[Complement factor I|Factor I]], inactivates C3b, the active form of C3. This process prevents the formation of C3 convertase and halts the progression of the complement cascade. C3-convertase also can be inhibited by [[decay accelerating factor]] (DAF), which is bound to erythrocyte plasma membranes via a [[Glycophosphatidylinositol|GPI]] anchor.<ref name=":2" />