Editing Complement system (section)

=== Complement deficiency ===
{{Main|Complement deficiency}}
It is thought that the complement system might play a role in many diseases with an immune component, such as [[Barraquer–Simons syndrome]], [[asthma]], [[lupus erythematosus]], [[glomerulonephritis]],  various forms of [[arthritis]], [[autoimmune heart disease]], [[multiple sclerosis]], [[inflammatory bowel disease]], [[paroxysmal nocturnal hemoglobinuria]], [[atypical hemolytic uremic syndrome]] and ischemia-reperfusion injuries,<ref name="pmid 15087815">{{Cite journal |vauthors=Arumugam TV, Shiels IA, Woodruff TM, Granger DN, Taylor SM |date=May 2004 |title=The role of the complement system in ischemia-reperfusion injury |journal=Shock |volume=21 |issue=5 |pages=401–9 |doi=10.1097/00024382-200405000-00002 |pmid=15087815 |s2cid=36655599 |doi-access=free}}</ref><ref name="pmid19443638">{{Cite journal |display-authors=6 |vauthors=Naesens M, Li L, Ying L, Sansanwal P, Sigdel TK, Hsieh SC, Kambham N, Lerut E, Salvatierra O, Butte AJ, Sarwal MM |date=August 2009 |title=Expression of complement components differs between kidney allografts from living and deceased donors |journal=Journal of the American Society of Nephrology |volume=20 |issue=8 |pages=1839–51 |doi=10.1681/ASN.2008111145 |pmc=2723986 |pmid=19443638}}</ref> and rejection of transplanted organs.<ref name="pmid 14499254">{{Cite journal |vauthors=Sacks SH, Chowdhury P, Zhou W |date=October 2003 |title=Role of the complement system in rejection |journal=Current Opinion in Immunology |volume=15 |issue=5 |pages=487–92 |doi=10.1016/S0952-7915(03)00100-6 |pmid=14499254}}</ref>

Complement regulation is suggested to play a role in pregnancy. Improper alternative complement pathway activation may mediate recurrent immune-mediated fetal loss.<ref>{{Cite journal |last1=Thurman |first1=Joshua M. |last2=Holers |first2=V. Michael |date=2006-02-01 |title=The Central Role of the Alternative Complement Pathway in Human Disease |url=https://journals.aai.org/jimmunol/article/176/3/1305/37524/The-Central-Role-of-the-Alternative-Complement |journal=The Journal of Immunology |language=en |volume=176 |issue=3 |pages=1305–1310 |doi=10.4049/jimmunol.176.3.1305 |pmid=16424154 |issn=0022-1767|url-access=subscription }}</ref><ref>{{Cite journal |last1=Mellor |first1=Andrew L. |last2=Sivakumar |first2=Jayabalan |last3=Chandler |first3=Phillip |last4=Smith |first4=Kimberly |last5=Molina |first5=Hector |last6=Mao |first6=Dailing |last7=Munn |first7=David H. |date=January 2001 |title=Prevention of T cell–driven complement activation and inflammation by tryptophan catabolism during pregnancy |url=https://www.nature.com/articles/ni0101_64 |journal=Nature Immunology |language=en |volume=2 |issue=1 |pages=64–68 |doi=10.1038/83183 |issn=1529-2908|url-access=subscription }}</ref>

The complement system is also becoming increasingly implicated in diseases of the central nervous system such as [[Alzheimer's disease]] and other neurodegenerative conditions such as spinal cord injuries.<ref>{{Cite journal |vauthors=Galvan MD, Luchetti S, Burgos AM, Nguyen HX, Hooshmand MJ, Hamers FP, Anderson AJ |date=December 2008 |title=Deficiency in complement C1q improves histological and functional locomotor outcome after spinal cord injury |journal=The Journal of Neuroscience |volume=28 |issue=51 |pages=13876–88 |doi=10.1523/JNEUROSCI.2823-08.2008 |pmc=2680920 |pmid=19091977}}</ref><ref>{{Cite journal |vauthors=Nguyen HX, Galvan MD, Anderson AJ |date=June 2008 |title=Characterization of early and terminal complement proteins associated with polymorphonuclear leukocytes in vitro and in vivo after spinal cord injury |journal=Journal of Neuroinflammation |volume=5 |pages=26 |doi=10.1186/1742-2094-5-26 |pmc=2443364 |pmid=18578885 |doi-access=free}}</ref><ref>{{Cite journal |vauthors=Beck KD, Nguyen HX, Galvan MD, Salazar DL, Woodruff TM, Anderson AJ |date=February 2010 |title=Quantitative analysis of cellular inflammation after traumatic spinal cord injury: evidence for a multiphasic inflammatory response in the acute to chronic environment |journal=Brain |volume=133 |issue=Pt 2 |pages=433–47 |doi=10.1093/brain/awp322 |pmc=2858013 |pmid=20085927}}</ref>

Deficiencies of the terminal pathway predispose to both [[autoimmune disease]] and [[infection]]s (particularly [[Neisseria meningitidis]], due to the role that the [[membrane attack complex]] ("MAC") plays in attacking [[Gram-negative]] bacteria).<ref>{{Cite book |title=Bacteria and Complement |vauthors=Brown EJ |date=1985 |publisher=Springer, Berlin, Heidelberg |isbn=9783642456060 |series=Current Topics in Microbiology and Immunology |volume=121 |pages=159–187 |language=en |chapter=Interaction of Gram-Positive Microorganisms with Complement |doi=10.1007/978-3-642-45604-6_8 |pmid=3936681}}</ref>

Infections with ''N. meningitidis'' and ''[[N. gonorrhoeae]]'' are the only conditions known to be associated with deficiencies in the MAC components of complement.<ref name="Ram2010">{{Cite journal |vauthors=Ram S, Lewis LA, Rice PA |date=October 2010 |title=Infections of people with complement deficiencies and patients who have undergone splenectomy |journal=Clinical Microbiology Reviews |volume=23 |issue=4 |pages=740–80 |doi=10.1128/CMR.00048-09 |pmc=2952982 |pmid=20930072}}</ref>  40–50% of those with MAC deficiencies experience recurrent infections with ''N. meningitidis''.<ref name="Lewis2014">{{Cite journal |vauthors=Lewis LA, Ram S |date=January 2014 |title=Meningococcal disease and the complement system |journal=Virulence |volume=5 |issue=1 |pages=98–126 |doi=10.4161/viru.26515 |pmc=3916388 |pmid=24104403}}</ref>