Complement system on the attack in autoimmunity.
The antiphospholipid syndrome is characterized clinically by fetal loss and thrombosis and serologically by the presence of autoantibodies to lipid-binding proteins. In a model of this procoagulant condition in which these antibodies are injected into pregnant mice, fetal loss was prevented by blocking of complement activation. Specifically, interaction of complement component 5a (C5a) with its receptor is necessary for thrombosis of placental vasculature. Inhibition of complement activation may have a therapeutic role in this disease.
Atkinson
John P
JP
Washington University School of Medicine, St. Louis, Missouri 63110-1093, USA. jatkinso@im.wustl.edu
D000022:Abortion, Spontaneous / Q000209:etiology*; D000818:Animals; D016736:Antiphospholipid Syndrome / Q000150:complications* / Q000276:immunology / Q000628:therapy; D001172:Arthritis, Rheumatoid / Q000150:complications / Q000276:immunology / Q000628:therapy; D015551:Autoimmunity; D003167:Complement Activation; D005260:Female; D051379:Mice; D009504:Neutrophils / Q000502:physiology*; D011247:Pregnancy; D011248:Pregnancy Complications / Q000276:immunology*; D044087:Receptor, Anaphylatoxin C5a / Q000502:physiology*
D044087:Receptor, Anaphylatoxin C5a