Early Classical Pathway Complement Proteins

While CML is blocked using complement inhibitory strategies, xenoantibodies continue to deposit on the graft endothelium, binding C1q and activating other uninhibited classical pathway complement proteins prior to C3. C1q binding facilitates cellular adhesion and ADCC, while C2b and C4a activation have proinflammatory effects. We hypothesize that the consequence of leaving this segment of the complement cascade functional is the enhancement of interactions with PBLs which lead to the development of proinflammatory and procoagulant events that contribute to AVXR. Monocytes, macrophages, B cells, neutrophils, platelets, and endothelial cells have C1q receptors (C1qR) which can facilitate their binding to endothelial cells following xenoantibody and C1q deposition.

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