Consecutive enzyme cascades: complement activation at the cell surface triggers increased tissue factor activity.
Complement activation at the cell surface initiates cell damage through a series of reactions occurring at the cell membrane and, after assembly of the terminal membrane attack complex, produces leakage of cytoplasmic contents from the cell. It has been documented that chemical or physical damage to cell membranes can cause a rapid increase in the expression of tissue factor procoagulant activity. In this study, antibody-mediated complement activation at the cell surface resulted in increased tissue factor activity, which correlated with cytolysis, as measured by 51-chromium release. Therefore, complement fixation on the cell surface can have a direct and immediate stimulatory effect on the coagulation cascade at the point of its initiation, with formation of a fibrin clot requiring only three consecutive proteolytic reactions after immunologically mediated cell damage.
Carson
S D
SD
Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha 68198-6495.
Johnson
D R
DR
D000906:Antibodies / Q000276:immunology; D002460:Cell Line; D002462:Cell Membrane / Q000276:immunology* / Q000502:physiology; D002857:Chromium / Q000378:metabolism; D003167:Complement Activation / Q000502:physiology*; D004797:Enzyme-Linked Immunosorbent Assay; D015942:Factor VIIa / Q000378:metabolism; D005170:Factor X / Q000378:metabolism; D005347:Fibroblasts / Q000276:immunology / Q000502:physiology; D006801:Humans; D007700:Kinetics; D013601:T-Lymphocytes / Q000276:immunology; D013925:Thromboplastin / Q000502:physiology*
D000906:Antibodies; D002857:Chromium; D005170:Factor X; D013925:Thromboplastin; D015942:Factor VIIa