Graft vascular endothelial cells (ECs) sense and respond to factors produced within both the circulation and parenchyma of a donor graft to mediate homeostatic regulation of critical physiologic factors including blood fluidity, vascular tone, and vessel wall permeability. 1 ECs also play an essential role in immune responses, acquiring new functions to regulate the progression and resolution of inflammation. 1 A breakdown in any of these EC functions-termed "EC dysfunction"-can contribute to the loss of transplanted organs.Moreover, because graft ECs are the first point of contact with the recipient immune system, many forms of post-transplant injury initiate at the EC surface, including ischemia reperfusion injury (IRI) and both acute and chronic rejection. 2,3 IRI-induced dysfunction leads to a loss of permselectivity, resulting in vascular leak. Vascular ECs can also participate in adaptive immunity by presenting antigens to circulating to T cells. Based on EC phenotype or activation state they may also trigger memory or regulatory T cell expression. 4 Thus, as a nexus of transplant pathology, graft ECs represent important therapeutic targets. However, there are currently no selective

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