Natural antibodies, autoantibodies and complement activation in tissue injury

Abstract

Ischemia/reperfusion-induced tissue damage is a significant problem occurring in multiple clinical conditions. Antibodies and complement activation contribute significantly to this pathology. Mice deficient in complement receptors 1 and 2 fail to produce a component of the natural antibody repertoire that binds to ischemia-conditioned tissues and activate complement. In contrast, mice prone to autoimmunity display accelerated tissue injury that results from the binding of autoantibodies to injured tissues. The specificity and production of natural antibodies, their role in autoimmunity and the mode of complement activation are reviewed from the perspective of the processes involved in ischemia/reperfusion-induced tissue damage.

• Natural antibodies
• autoantibodies
• complement activation
• reperfusion injury
• ischemia

Acknowledgements

This work was supported by the following NIH NCRR Grant P20 RR017686 and RR016475, US Army contract, Terry C Johnson Center for Cancer Research, NSF Grant No. SBE-0244984, and the Division of Biology. Its contents are solely the responsibility of the authors and do not necessarily represent the official views of NIH. I would like to thank Dr S.K. Chapes for critical reading and discussion of the manuscript and Sara M. Hoffman for help with the figures.