The JI PBL Intereron Source
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     
 


The Journal of Immunology, 1979, 123: 2421-2427.
Copyright © 1979 by The American Association of Immunologists, Inc.

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Goldman, J. N.
Right arrow Articles by Goldman, M. B.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Goldman, J. N.
Right arrow Articles by Goldman, M. B.

Activation of Murine Complement by Cobra Venom Factor in the Presence of EDTA1

John N. Goldman, Shrikar Bangalore and Margaret B. Goldman

From the Departments of Medicine and Pathology, Michael Reese Medical Center and the Pritzker School of Medicine, University of Chicago, Chicago, Illinois 60616

Abstract

The anticomplementary factor of cobra venom (CoVF) was found to activate the terminal complement (C) components (C5 through C9) in mouse or rat serum or plasma in the presence of EDTA. The same concentrations of EDTA would block C activation by EA, zymosan, and inulin and would block C activation in human and guinea pig serum by all of these activators, including CoVF. Murine serum was found to contain two factors that allowed CoVF-induced C activation and bystander hemolysis in the presence of EDTA. The first was factor B or a related component of the alternative pathway, which allowed formation of a functionally active complex of CoVF and factor B in the presence of EDTA. The second was murine C5, which led to augmented hemolysis of unsensitized bystander erythrocytes and activation of the other terminal components. Preformed complexes of CoVF and rat factor B were active in leading to C5 and C6 consumption in human or guinea pig serum that had been fortified with rat C5. In contrast to native CoVF, these complexes did not lead to electrophoretic conversion of C3 in the human or guinea pig serum. It was further shown that in the presence of rat C5, purified CoVF led to moderate activation of the terminal components in human serum-EDTA in the absence of electrophoretic conversion of C3, indicating that in these situations, CoVF activated C5 and the other terminal components with little or no utilization of C3.

Footnotes

1 This work was supported by Research Grant AI 12792 from the National Institutes of Health and by the Medical Research Institute Council, Michael Reese Medical Center.




This article has been cited by other articles:


Home page
Proc. Natl. Acad. Sci. USAHome page
Y. Xu, M. Ma, G. C. Ippolito, H. W. Schroeder Jr., M. C. Carroll, and J. E. Volanakis
Complement activation in factor D-deficient mice
PNAS, November 20, 2001; (2001) 261428398.
[Abstract] [Full Text] [PDF]


Home page
Proc. Natl. Acad. Sci. USAHome page
Y. Xu, M. Ma, G. C. Ippolito, H. W. Schroeder Jr., M. C. Carroll, and J. E. Volanakis
Complement activation in factor D-deficient mice
PNAS, December 4, 2001; 98(25): 14577 - 14582.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Website Copyright © 1979 by The American Association of Immunologists, Inc. All rights reserved.
All Contents Copyright © 1979 by The American Association of Immunologists, Inc. All rights reserved.