Editing Factor XII (section)

== Clinical significance ==
{{main|Factor XII deficiency}}
Factor XII deficiency is a rare disorder that is inherited in an [[autosomal recessive]] manner.<ref name=Wagenman>{{cite journal | vauthors = Wagenman BL, Townsend KT, Mathew P, Crookston KP | title = The laboratory approach to inherited and acquired coagulation factor deficiencies | journal = Clinics in Laboratory Medicine | volume = 29 | issue = 2 | pages = 229–252 | date = June 2009 | pmid = 19665676 | doi = 10.1016/j.cll.2009.04.002 | url = https://zenodo.org/record/894920 }}</ref> Unlike other clotting factor deficiencies, factor XII deficiency is totally asymptomatic and does not cause excess bleeding.<ref name=Wagenman /> Mice lacking the gene for factor XII, however, are less susceptible to [[thrombosis]]. The protein seems to be involved in the later stages of clot formation rather than the first occlusion of damages in the blood vessel wall.<ref name="pmid16009717">{{cite journal | vauthors = Renné T, Pozgajová M, Grüner S, Schuh K, Pauer HU, Burfeind P, Gailani D, Nieswandt B | title = Defective thrombus formation in mice lacking coagulation factor XII | journal = The Journal of Experimental Medicine | volume = 202 | issue = 2 | pages = 271–281 | date = July 2005 | pmid = 16009717 | pmc = 2213000 | doi = 10.1084/jem.20050664 }}</ref>

Factor XII does play an important role in clot formation during ''in vitro'' measurements of the [[partial thromboplastin time]], which causes these measurements to be markedly prolonged in patients with factor XII deficiency, usually well beyond even what is seen in hemophilia A, hemophilia B, or factor XI deficiency.<ref name=Wagenman /> As a result, the main concern related to factor XII deficiency is the unnecessary testing, delay in care, worry, etc. that may be prompted by the abnormal lab result.<ref name=Wagenman /> All of this, including the mechanism of inheritance, also holds true for the other contact factors, [[prekallikrein]] (Fletcher factor) and high molecular weight [[kininogen]].<ref name=Wagenman />

Excess levels of factor XII can predispose individuals towards greater risk of [[venous thrombosis]] due to factor XII's role as one of the catalysts for conversion of plasminogen to its active fibrinolytic form of [[plasmin]].<ref name=isbn0-86542-446-2>{{cite book |title= Manual of Coagulation Disorders| vauthors = Kroll MH |year= 2001|publisher= Blackwell Science|isbn= 0-86542-446-2|pages= 3–4, 206–207}}</ref>

Factor XII is also activated by [[endotoxin]]s, especially [[lipid A]] in vitro. Experimental mouse models have suggested a role of FXII in multiple sclerosis.<ref name="pmid">{{cite journal | vauthors = Göbel K, Pankratz S, Asaridou CM, Herrmann AM, Bittner S, Merker M, Ruck T, Glumm S, Langhauser F, Kraft P, Krug TF, Breuer J, Herold M, Gross CC, Beckmann D, Korb-Pap A, Schuhmann MK, Kuerten S, Mitroulis I, Ruppert C, Nolte MW, Panousis C, Klotz L, Kehrel B, Korn T, Langer HF, Pap T, Nieswandt B, Wiendl H, Chavakis T, Kleinschnitz C, Meuth SG | title = Blood coagulation factor XII drives adaptive immunity during neuroinflammation via CD87-mediated modulation of dendritic cells | journal = Nature Communications | volume = 7 | issue =  | pages = 11626 | date = May 2016 | pmid =  27188843| pmc = 4873982 | doi = 10.1038/ncomms11626 | bibcode = 2016NatCo...711626G }}</ref>