1. Anti-mouse properdin TSR 5/6 monoclonal antibodies block complement alternative pathway-dependent pathogenesis.
- Author
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Bertram P, Akk AM, Zhou HF, Mitchell LM, Pham CT, and Hourcade DE
- Subjects
- Animals, Antibodies, Monoclonal biosynthesis, Aortic Aneurysm, Abdominal chemically induced, Aortic Aneurysm, Abdominal immunology, Aortic Aneurysm, Abdominal pathology, Cricetinae, Escherichia coli genetics, Escherichia coli metabolism, Female, Gene Expression, Immunosuppressive Agents metabolism, Mice, Mice, Inbred C57BL, Pancreatic Elastase, Properdin genetics, Properdin immunology, Rabbits, Recombinant Proteins biosynthesis, Recombinant Proteins pharmacology, Antibodies, Monoclonal pharmacology, Aortic Aneurysm, Abdominal prevention & control, Complement Pathway, Alternative drug effects, Immunosuppressive Agents pharmacology, Properdin antagonists & inhibitors
- Abstract
The complement alternative pathway (AP) is a major contributor to a broad and growing spectrum of diseases that includes age-related macular degeneration, atypical hemolytic uremic syndrome, and preeclampsia. As a result, there is much interest in the therapeutic disruption of AP activity. Properdin, the only positive regulator of the AP, is a particularly promising AP target. Several issues need to be clarified before the potential for properdin-directed therapy can be realized. In this report we use a portion of the mouse properdin protein, expressed in a bacterial system, to raise rabbit polyclonal and hamster monoclonal antibodies that block properdin-dependent pathogenesis. These antibodies, when employed with AP-dependent mouse disease models, can help evaluate the feasibility of properdin-directed therapy.
- Published
- 2015
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