期刊
FRONTIERS IN IMMUNOLOGY
卷 3, 期 -, 页码 -出版社
FRONTIERS RESEARCH FOUNDATION
DOI: 10.3389/fimmu.2012.00341
关键词
ischemia; reperfusion; MBL; kidney; complement
类别
资金
- Medical Research Council [G0600892, MR/J006742/1, G1001197] Funding Source: researchfish
- Medical Research Council [G0801952, G0600892, G1001197, G0700859, G0501425, MR/J006742/1, G1000191] Funding Source: Medline
- MRC [G1001197, G0501425, G0700859, G0600892, G1000191, G0801952] Funding Source: UKRI
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.
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