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Combination cell therapy leads to clonal deletion of donor-specific T cells in kidney transplant recipients.
EBioMedicine
August 2024
Division of Nephrology and Dialysis, Department of Medicine III, Medical University of Vienna, Vienna, Austria. Electronic address:
Background: Induction of donor-specific tolerance is a promising approach to achieve long-term graft patency in transplantation with little to no maintenance immunosuppression. Changes to the recipient's T cell receptor (TCR) repertoire are understood to play a pivotal role in the establishment of a robust state of tolerance in chimerism-based transplantation protocols.
Methods: We investigated changes to the TCR repertoires of patients participating in an ongoing prospective, controlled, phase I/IIa trial designed to evaluate the safety and efficacy of combination cell therapy in living donor kidney transplantation.
Chimerism-Based Tolerance to Kidney Allografts in Humans: Novel Insights and Future Perspectives.
Front Immunol
February 2022
Columbia Center for Translational Immunology, Department of Medicine, Department of Surgery, Department of Microbiology and Immunology, Columbia University, New York, NY, United States.
Chronic rejection and immunosuppression-related toxicity severely affect long-term outcomes of kidney transplantation. The induction of transplantation tolerance - the lack of destructive immune responses to a transplanted organ in the absence of immunosuppression - could potentially overcome these limitations. Immune tolerance to kidney allografts from living donors has been successfully achieved in humans through clinical protocols based on chimerism induction with hematopoietic cell transplantation after non-myeloablative conditioning.
View Article and Find Full Text PDFMemory T cell-mediated rejection is mitigated by FcγRIIB expression on CD8 T cells.
Am J Transplant
August 2020
Department of Surgery, Emory Transplant Center, Emory University School of Medicine, Atlanta, Georgia.
Donor-reactive memory T cells generated via heterologous immunity represent a potent barrier to long-term graft survival following transplantation because of their increased precursor frequency, rapid effector function, altered trafficking patterns, and reduced reliance on costimulation signals for activation. Thus, the identification of pathways that control memory T cell survival and secondary recall potential may provide new opportunities for therapeutic intervention. Here, we discovered that donor-specific effector/memory CD8 T cell populations generated via exposure to acute vs latent vs chronic infections contain differential frequencies of CD8 T cells expressing the inhibitory Fc receptor FcγRIIB.
View Article and Find Full Text PDFDeletion of donor-reactive T cell clones after human liver transplant.
Am J Transplant
February 2020
Columbia Center for Translational Immunology, Department of Medicine, Columbia University Medical Center, New York, New York.
We recently developed a high throughput T cell receptor β chain (TCRβ) sequencing-based approach to identifying and tracking donor-reactive T cells. To address the role of clonal deletion in liver allograft tolerance, we applied this method in samples from a recent randomized study, ITN030ST, in which immunosuppression withdrawal was attempted within 2 years of liver transplantation. We identified donor-reactive T cell clones via TCRβ sequencing following a pre-transplant mixed lymphocyte reaction and tracked these clones in the circulation following transplantation in 3 tolerant and 5 non-tolerant subjects.
View Article and Find Full Text PDFTransplantation tolerance in nonhuman primates and humans.
Bone Marrow Transplant
August 2019
Columbia Center for Translational Immunology, Columbia University Medical Center, New York, NY, USA.
This review focuses on our recent studies involving nonmyeloablative bone marrow transplantation as an approach to inducing organ allograft tolerance across MHC barriers in nonhuman primates and in patients. The clinical studies are focused on mechanisms of tolerance involved in a protocol carried out at Massachusetts General Hospital in HLA-mismatched haploidentical combinations for the induction of renal allograft tolerance. These studies, in which chimerism was only transient and GVHD did not occur, suggest an early role for donor-specific regulatory T cells in tolerance induction, followed by partial and gradual deletion of donor-reactive T cells.
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