Complement activation by whole endotoxin is blocked by a monoclonal antibody to factor B.
Sepsis is both a common and, despite present-day therapy, a serious disease. The pathophysiology of the septic response is a complex, multifactorial phenomenon which in part involves the activation of complement by bacterial endotoxin. A monoclonal antibody to human complement factor B, code-named 1H5, which was capable of specifically inhibiting the alternative pathway of complement activation at concentrations as low as 1 microgram/ml, is described. This agent had no effect on the classical pathway of complement activation. It was capable of preventing the activation of complement by even high concentrations (0.1 mg/ml) of whole endotoxin; however, it was ineffective in preventing activation of complement by endotoxin derived from a rough mutant. This agent could potentially be used in the treatment of sepsis.
Clardy
C W
CW
Department of Pediatrics, Rush Medical College, Chicago, Illinois 60612.
D000818:Animals; D000911:Antibodies, Monoclonal / Q000276:immunology*; D003167:Complement Activation / Q000187:drug effects*; D011415:Complement Factor B / Q000502:physiology*; D004731:Endotoxins / Q000633:toxicity*; D005260:Female; D051379:Mice; D008807:Mice, Inbred BALB C
D000911:Antibodies, Monoclonal; D004731:Endotoxins; D011415:Complement Factor B