The Cytolytic C5b-9 Complement Complex: Feedback Inhibition of Complement Activation

We describe a regulatory function of the terminal cytolytic C5b-9 complex [C5b-9(m)] of human complement. Purified C5b-9(m) complexes isolated from target membranes, whether in solution or bound to liposomes, inhibited lysis of sensitized sheep erythrocytes by whole human serum in a dose-dependent m... Ausführliche Beschreibung

1. Person: Bhakdi, Sucharit
Weitere Personen: Maillet, Françoise verfasserin; Muhly, Marion verfasserin; Kazatchkine, Michel D. verfasserin
Quelle: in Proceedings of the National Academy of Sciences of the United States of America Vol. 85, No. 6 (1988), p. 1912-1916
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Format: Online-Artikel
Sprache: English
Veröffentlicht: 1988
Beschreibung: Online-Ressource
Schlagworte: research-article
Immunology
Complement Regulation
C3 Convertase Formation
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Zusammenfassung: We describe a regulatory function of the terminal cytolytic C5b-9 complex [C5b-9(m)] of human complement. Purified C5b-9(m) complexes isolated from target membranes, whether in solution or bound to liposomes, inhibited lysis of sensitized sheep erythrocytes by whole human serum in a dose-dependent manner. C9 was not required for the inhibitory function since C5b-7 and C5b-8 complexes isolated from membranes were also effective. No effect was found with the cytolytically inactive, fluid-phase SC5b-9 complex. However, tryptic modification of SC5b-9 conferred an inhibitory capacity to the complex, due probably to partial removal of the S protein. Experiments using purified components demonstrated that C5b-9(m) exerts a regulatory effect on the formation of the classical- and alternative-pathway C3 convertases and on the utilization of C5 by cell-bound C5 convertases. C5b-9(m) complexes were unable to inhibit the lysis of cells bearing C5b-7(m) by C8 and C9. Addition of C5b-9(m) to whole human serum abolished its bactericidal effect on the serum-sensitive Escherichia coli K-12 strain W 3110 and suppressed its hemolytic function on antibody-sensitized, autologous erythrocytes. Feedback inhibition by C5b-9(m) represents a biologically relevant mechanism through which complement may autoregulate its effector functions.
ISSN: 0027-8424

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