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. Author manuscript; available in PMC: 2020 Mar 1.
Published in final edited form as: Clin Lab Med. 2018 Dec 20;39(1):31–43. doi: 10.1016/j.cll.2018.10.004

Figure 2. Mechanisms through which complement mediates ischemia-reperfusion injury.

Figure 2.

Hypoxia induces surface expression of neoantigens that are recognized by natural, pre-formed IgM and MBL (and/or collectins), which then initiate complement activation. Following reperfusion, the generation of reactive oxygen species (ROS) is associated with graft-derived complement production and activation as well as the release of damage-associated molecular patterns (DAMPs). Subsequent Toll-like receptor (TLR) signaling synergizes with and amplifies complement activation, together yielding C3a and C5a. These anaphylatoxins signal through their 7-transmembrane spanning G-protein coupled receptors on endothelial cells (among other cellular targets) inducing cytokine/chemokine release and facilitating T cell infiltration into the allograft.