Journal
IMMUNOLOGIC RESEARCH
Volume 47, Issue 1-3, Pages 25-44Publisher
HUMANA PRESS INC
DOI: 10.1007/s12026-009-8136-3
Keywords
Alloantibody; Complement; Ig knockout mice; Cardiac rejection; vWf; C4d; MBL; Fc gamma and complement receptors; Endothelial cells; Macrophages
Categories
Funding
- NIH [R01-HL63948]
- American Heart Association
- Roche Organ Transplantation Research Foundation (ROTRF) [508303540, 513443778]
- Talecris Biotherapeutics, Inc.
- Talent Program
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Antibody-mediated rejection has become critical clinically because this form of rejection is usually unresponsive to conventional anti-rejection therapy, and therefore, it has been recognized as a major cause of allograft loss. Our group developed experimental animal models of vascularized organ transplantation to study pathogenesis of antibody- and complement-mediated endothelial cell injury leading to graft rejection. In this review, we discuss mechanisms of antibody-mediated graft rejection resulting from activation of complement by C1q- and MBL (mannose-binding lectin)-dependent pathways and interactions with a variety of effector cells, including macrophages and monocytes through Fc gamma receptors and complement receptors.
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