Live-donor transplantation after desensitization provided a significant survival benefit for patients with HLA sensitization, as compared with waiting for a compatible organ. By 8 years, this survival advantage more than doubled. These data provide evidence that desensitization protocols may help overcome incompatibility barriers in live-donor renal transplantation. (Funded by the National Institute of Diabetes and Digestive and Kidney Diseases and the Charles T. Bauer Foundation.).

Adaptors are molecular scaffolds that recruit effectors, which are critical for immune cell activation. Recent work has underscored the requirement for adaptors in propagating stimulatory signals as well as their ability to inhibit immune cell function. The mechanisms by which adaptors function rely not only on the intermolecular interactions they mediate, but also on where they are localized within the cell. The use of sophisticated genetic, biochemical, cellular and imaging approaches has provided important new insights into the biology of adaptor protein function. Here we focus on T lymphocytes as a model to illustrate the critical roles adaptors play as regulators of cellular activation.

Desensitized patients are at high risk of developing acute antibody-mediated rejection (AMR). In most cases, the rejection episodes are mild and respond to a short course of plasmapheresis (PP) / low-dose IVIg treatment. However, a subset of patients experience severe AMR associated with sudden onset oliguria. We previously described the utility of emergent splenectomy in rescuing allografts in patients with this type of severe AMR. However, not all patients are good candidates for splenectomy. Here we present a single case in which eculizumab, a complement protein C5 antibody that inhibits the formation of the membrane attack complex (MAC), was used combined with PP/IVIg to salvage a kidney undergoing severe AMR. We show a marked decrease in C5b-C9 (MAC) complex deposition in the kidney after the administration of eculizumab.