Please use this identifier to cite or link to this item: http://hdl.handle.net/2381/38281
Title: Which pathways trigger the role of complement in ischaemia/reperfusion injury?
Authors: Farrar, C. A.
Asgari, E.
Schwaeble, Wilhelm J.
Sacks, S. H.
First Published: 19-Nov-2012
Citation: Frontiers in Immunology, 2012, 3, pp. 341-?
Abstract: Investigations into the role of complement in ischemia/reperfusion (I/R) injury have identified common effector mechanisms that depend on the production of C5a and C5b-9 through the cleavage of C3. These studies have also defined an important role for C3 synthesized within ischemic kidney. Less clear however is the mechanism of complement activation that leads to the cleavage of C3 in ischemic tissues and to what extent the potential trigger mechanisms are organ dependent - an important question which informs the development of therapies that are more selective in their ability to limit the injury, yet preserve the other functions of complement where possible. Here we consider recent evidence for each of the three major pathways of complement activation (classical, lectin, and alternative) as mediators of I/R injury, and in particular highlight the role of lectin molecules that increasingly seem to underpin the injury in different organ models and in addition reveal unusual routes of complement activation that contribute to organ damage.
DOI Link: 10.3389/fimmu.2012.00341
eISSN: 1664-3224
Links: http://journal.frontiersin.org/article/10.3389/fimmu.2012.00341/
http://hdl.handle.net/2381/38281
Version: Publisher Version
Status: Peer-reviewed
Type: Journal Article
Rights: © 2012 Farrar, Asgari, Schwaeble and Sacks. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in other forums, provided the original authors and source are credited and subject to any copyright notices concerning any third-party graphics etc.
Appears in Collections:Published Articles, Dept. of Infection, Immunity and Inflammation

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