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2025

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1977 1
1980 1
1981 1
1983 1
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2000 1
2008 1
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2017 1
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2025 0

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13 results

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Page 1
Paroxysmal nocturnal haemoglobinuria.
Hill A, DeZern AE, Kinoshita T, Brodsky RA. Hill A, et al. Nat Rev Dis Primers. 2017 May 18;3:17028. doi: 10.1038/nrdp.2017.28. Nat Rev Dis Primers. 2017. PMID: 28516949 Free PMC article. Review.
The gene product of PIGA is required for the biosynthesis of glycosylphosphatidylinositol (GPI) anchors; thus, PIGA mutations lead to a deficiency of GPI-anchored proteins, such as complement decay-accelerating factor (also known as CD55) and CD59 glycoprotein (CD59), whic …
The gene product of PIGA is required for the biosynthesis of glycosylphosphatidylinositol (GPI) anchors; thus, PIGA mutations lead to a d
Complement and periodontitis.
Hajishengallis G. Hajishengallis G. Biochem Pharmacol. 2010 Dec 15;80(12):1992-2001. doi: 10.1016/j.bcp.2010.06.017. Epub 2010 Jun 23. Biochem Pharmacol. 2010. PMID: 20599785 Free PMC article. Review.
Clinical and histological observations show a correlation between periodontal inflammatory activity and local complement activation. Certain genetic polymorphisms or deficiencies in specific complement components appear to predispose to increased susceptibility to periodon …
Clinical and histological observations show a correlation between periodontal inflammatory activity and local complement activation. Certain …
Complement regulation of T-cell alloimmunity.
Cravedi P, van der Touw W, Heeger PS. Cravedi P, et al. Semin Nephrol. 2013 Nov;33(6):565-74. doi: 10.1016/j.semnephrol.2013.08.007. Semin Nephrol. 2013. PMID: 24161041 Free PMC article. Review.
The immune cell-derived, alternative pathway complement components activate spontaneously, yielding local, but not systemic, production of C3a and C5a. These anaphylatoxins bind to their respective G-protein-coupled receptors, the C3a receptor and the C5a receptor, express …
The immune cell-derived, alternative pathway complement components activate spontaneously, yielding local, but not systemic, production of C …
The Role of Complement C3a Receptor in Stroke.
Ahmad S, Bhatia K, Kindelin A, Ducruet AF. Ahmad S, et al. Neuromolecular Med. 2019 Dec;21(4):467-473. doi: 10.1007/s12017-019-08545-7. Epub 2019 May 17. Neuromolecular Med. 2019. PMID: 31102134 Review.
The C3a anaphylatoxin, via its cognate C3a receptor (C3aR), mediates inflammation by promoting breakdown of the blood-brain barrier and the massive infiltration of leukocytes into ischemic brain in experimental stroke models. Studies utilizing complement deficient mice as …
The C3a anaphylatoxin, via its cognate C3a receptor (C3aR), mediates inflammation by promoting breakdown of the blood-brain barrier and the …
Coagulation inhibitor substitution during sepsis.
Fourrier F, Jourdain M, Tournois A, Caron C, Goudemand J, Chopin C. Fourrier F, et al. Intensive Care Med. 1995 Nov;21 Suppl 2:S264-8. doi: 10.1007/BF01740765. Intensive Care Med. 1995. PMID: 8636534 Review.
Activation of the contact system induces activation of the classical complement pathway with generation of anaphylatoxins, of the kinins pathway and of fibrinolysis. Physiologic inhibition depends on the C1-inhibitor (C1-Inh.). Septic patients exhibit a relative deficie
Activation of the contact system induces activation of the classical complement pathway with generation of anaphylatoxins, of the kin …
Complement inhibition keeps mothers calm and avoids fetal rejection.
Girardi G. Girardi G. Immunol Invest. 2008;37(5):645-59. doi: 10.1080/08820130802191615. Immunol Invest. 2008. PMID: 18716942 Review.
Complement activation caused dysregulation of the angiogenic factors (deficiency of free vascular endothelial growth factor (VEGF) and elevated levels of soluble VEGF receptor 1) required for normal placental development. ...
Complement activation caused dysregulation of the angiogenic factors (deficiency of free vascular endothelial growth factor (VEGF) an …
Controlling the complement system in inflammation.
Kirschfink M. Kirschfink M. Immunopharmacology. 1997 Dec;38(1-2):51-62. doi: 10.1016/s0162-3109(97)00057-x. Immunopharmacology. 1997. PMID: 9476114 Review.
These consequences are clinically manifested in various disorders, including septic shock, multiple organ failure and hyperacute graft rejection. Genetic complement deficiencies or complement depletion have been proven to be beneficial in reducing tissue injury in a number …
These consequences are clinically manifested in various disorders, including septic shock, multiple organ failure and hyperacute graft rejec …
The role of complement in urticaria and angioedema.
Gelfand JA. Gelfand JA. Clin Immunol Rev. 1981-1982;1(2):257-309. Clin Immunol Rev. 1981. PMID: 6762276 Review.
As we have seen, the absence of inhibitor proteins, such as ClINH, C3bINA, or Carboxypeptidase N Anaphylatoxin Inactivator) can permit small amounts of active complement fragments, liberated "normally" through the action of nonspecific effector pathways, to produce general …
As we have seen, the absence of inhibitor proteins, such as ClINH, C3bINA, or Carboxypeptidase N Anaphylatoxin Inactivator) can permi …
C1-Esterase inhibitor: an anti-inflammatory agent and its potential use in the treatment of diseases other than hereditary angioedema.
Caliezi C, Wuillemin WA, Zeerleder S, Redondo M, Eisele B, Hack CE. Caliezi C, et al. Pharmacol Rev. 2000 Mar;52(1):91-112. Pharmacol Rev. 2000. PMID: 10699156 Review.
A typical feature of the contact and complement system is that on activation they give rise to vasoactive peptides such as bradykinin or the anaphylatoxins, which in part explains the proinflammatory effects of either system. C1-Inh, belonging to the superfamily of serine …
A typical feature of the contact and complement system is that on activation they give rise to vasoactive peptides such as bradykinin or the …
C1-inhibitor substitution therapy in septic shock and in the vascular leak syndrome induced by high doses of interleukin-2.
Hack CE, Ogilvie AC, Eisele B, Eerenberg AJ, Wagstaff J, Thijs LG. Hack CE, et al. Intensive Care Med. 1993;19 Suppl 1:S19-28. doi: 10.1007/BF01738946. Intensive Care Med. 1993. PMID: 8053997 Review.
Functional levels of C1-INH tend to be normal in septic patients although paradoxically this inhibitor is an acute phase protein. Moreover, levels of proteolytically inactivated C1-INH are increased in sepsis pointing to an increased turn-over. These observations suggest a …
Functional levels of C1-INH tend to be normal in septic patients although paradoxically this inhibitor is an acute phase protein. Moreover, …
13 results