PD-L1's Role in Preventing Alloreactive T Cell Responses Following Hematopoietic and Organ Transplant

Over the past decade, Programmed Death-Ligand 1 (PD-L1) has emerged as a prominent target for cancer immunotherapies. However, its potential as an immunosuppressive therapy has been limited. In this review, we present the immunological basis of graft rejection and graft-versus-host disease (GVHD), followed by a summary of biologically relevant molecular interactions of both PD-L1 and Programmed Cell Death Protein 1 (PD-1). Finally, we present a translational perspective on how PD-L1 can interrupt alloreactive-driven processes to increase immune tolerance. Unlike most current therapies that block PD-L1 and/or its interaction with PD-1, this review focuses on how upregulation or reversed sequestration of this ligand may reduce autoimmunity, ameliorate GVHD, and enhance graft survival following organ transplant.

Automated summary

Over the past decade, PD-L1 has become a prominent target in cancer immunotherapies, but its potential as an immunosuppressive therapy has been limited. This review presents the immunological basis of graft rejection and GVHD, and summarizes the molecular interactions of PD-L1 and PD-1. It also provides a translational perspective on how manipulating PD-L1 can increase immune tolerance and improve graft survival.