Publications

Abstract

PURPOSE OF REVIEW: Clinical islet transplantation does not enjoy the success seen for solid organ transplants, indicating a need for new therapeutic approaches to improve patient outcomes. This has prompted investigation into islet autonomous factors and pathways that may represent druggable targets. These have the potential to synergize with approaches aimed at generating graft-specific tolerance. RECENT FINDINGS: There are emerging data that nuclear factor kappaB (NF-kappaB) activation can prevent and or overcome tolerance, whereas dampening NF-kappaB activation in immune cells is associated with prolonged allograft survival. In islet cells, NF-kappaB plays a central role in triggering the inflammatory transcriptional response that is often associated with reduced islet function and contributes to poor transplant outcomes. SUMMARY: Targeting intraislet NF-kappaB represents a promising target in islet transplantation. Here we will discuss the current state of the knowledge on the role of NF-kappaB activation in the context of islet transplantation and the implications of targeting NF-kappaB for tolerance induction.