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Clonal dynamics of alloreactive T cells in kidney allograft rejection after anti-PD-1 therapy

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE216763 | GEO | 2023/02/01

REPOSITORIES: GEO

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Clonal dynamics of alloreactive T cells in kidney allograft rejection after anti-PD-1 therapy.

Project description:Kidney transplant recipients are at particular risk for developing tumors, many of which are now routinely treated with immune checkpoint inhibitors (ICIs); however, ICI therapy can precipitate transplant rejection. Here, we use TCR sequencing to identify and track alloreactive T cells in a patient with melanoma who experienced kidney transplant rejection following PD-1 inhibition. The treatment was associated with a sharp increase in circulating alloreactive CD8+ T cell clones, which display a unique transcriptomic signature and were also detected in the rejected kidney but not at tumor sites. Longitudinal and cross-tissue TCR analyses indicate unintended expansion of alloreactive CD8+ T cells induced by ICI therapy for cancer, coinciding with ICI-associated organ rejection.

| S-EPMC10027853 | biostudies-literature

Clonal dynamics of alloreactive T cells in kidney allograft rejection after anti-PD-1 therapy [bulkTCRseq]

Project description:Kidney transplant recipients are at particular risk for developing tumors, many of which are now routinely treated with immune checkpoint inhibitors (ICIs); however, ICI therapy can precipitate transplant rejection. We utilized TCR sequencing to identify and track alloreactive T cells in a patient with melanoma who experienced kidney transplant rejection following ICI therapy. ICI therapy was associated with a sharp increase in circulating alloreactive CD8+ T cell clones, many of which were also detected in the rejected kidney but not at tumor sites. Longitudinal and cross-tissue TCR analyses revealed unintended expansion of alloreactive CD8+ T cells induced by ICI therapy for cancer, coinciding with ICI-associated organ rejection.

2023-02-01 | GSE216758 | GEO

Clonal dynamics of alloreactive T cells in kidney allograft rejection after anti-PD-1 therapy [MLR single-cell]

Project description:Kidney transplant recipients are at particular risk for developing tumors, many of which are now routinely treated with immune checkpoint inhibitors (ICIs); however, ICI therapy can precipitate transplant rejection. We utilized TCR sequencing to identify and track alloreactive T cells in a patient with melanoma who experienced kidney transplant rejection following ICI therapy. ICI therapy was associated with a sharp increase in circulating alloreactive CD8+ T cell clones, many of which were also detected in the rejected kidney but not at tumor sites. Longitudinal and cross-tissue TCR analyses revealed unintended expansion of alloreactive CD8+ T cells induced by ICI therapy for cancer, coinciding with ICI-associated organ rejection.

2023-02-01 | GSE216756 | GEO

Clonal dynamics of alloreactive T cells in kidney allograft rejection after anti-PD-1 therapy [Non-naive CD8 single-cell]

Project description:Kidney transplant recipients are at particular risk for developing tumors, many of which are now routinely treated with immune checkpoint inhibitors (ICIs); however, ICI therapy can precipitate transplant rejection. We utilized TCR sequencing to identify and track alloreactive T cells in a patient with melanoma who experienced kidney transplant rejection following ICI therapy. ICI therapy was associated with a sharp increase in circulating alloreactive CD8+ T cell clones, many of which were also detected in the rejected kidney but not at tumor sites. Longitudinal and cross-tissue TCR analyses revealed unintended expansion of alloreactive CD8+ T cells induced by ICI therapy for cancer, coinciding with ICI-associated organ rejection.

2023-02-01 | GSE216762 | GEO

Clonal dynamics of alloreactive T cells in kidney allograft rejection after anti-PD-1 therapy

Project description:Clonal dynamics of alloreactive T cells in kidney allograft rejection after anti-PD-1 therapy

| PRJNA895342 | ENA

Clonal dynamics of alloreactive T cells in kidney allograft rejection after anti-PD-1 therapy [bulkTCRseq]

Project description:Clonal dynamics of alloreactive T cells in kidney allograft rejection after anti-PD-1 therapy [bulkTCRseq]

| PRJNA895346 | ENA

Clonal dynamics of alloreactive T cells in kidney allograft rejection after anti-PD-1 therapy [MLR single-cell]

Project description:Clonal dynamics of alloreactive T cells in kidney allograft rejection after anti-PD-1 therapy [MLR single-cell]

| PRJNA895336 | ENA

Clonal dynamics of alloreactive T cells in kidney allograft rejection after anti-PD-1 therapy [Non-naive CD8 single-cell]

Project description:Clonal dynamics of alloreactive T cells in kidney allograft rejection after anti-PD-1 therapy [Non-naive CD8 single-cell]

| PRJNA895347 | ENA

Kidney retransplantation after anti-programmed cell death-1 (PD-1)-related allograft rejection.

Project description:In this report, we describe the first kidney retransplantation performed after anti-programmed cell death-1 (PD-1)-related allograft rejection. In 2014, we administered pembrolizumab (anti-PD-1) for ~9 months to a 57-year-old kidney transplant recipient with metastatic cutaneous squamous cell carcinoma (CSCC). The patient experienced both a complete antitumor response and T cell-mediated allograft rejection requiring reinitiation of hemodialysis. Four-and-a-half years after initiating pembrolizumab, the patient remained without evidence of CSCC relapse and received a kidney transplant from a living-unrelated donor. Ten-and-a-half months after kidney retransplantation, the allograft is functioning well and the patient's CSCC remains in remission. This case illustrates the potential for PD-1 blockade to bring about durable immune-mediated tumor control in chronically immunosuppressed patients, and begins to address the feasibility of kidney retransplantation in patients who have previously received immune checkpoint inhibitor therapy for cancer. Results from this and future cases may help elucidate mechanisms of antitumor immunity and allograft tolerance, and inform updates to transplant decision models. Our report also underscores the need for clinical trials testing novel immunotherapy combinations in solid organ transplant recipients designed to uncouple antitumor and anti-allograft immunity.

| S-EPMC7395855 | biostudies-literature

Association between anti-endothelial antigen antibodies and allograft rejection in kidney transplantation.

Project description:BackgroundEndothelial cells are vital in the transplant immune system as semiprofessional antigen-presenting cells. Few studies have investigated the importance of anti-endothelin subtype A receptor (ETAR) antibodies in kidney transplantation. Here, we aimed to analyze the association between anti-angiotensin II type I receptor (AT1R) and anti-ETAR antibodies and the association between the presence of anti-endothelial antibodies and the risk of allograft rejection in kidney transplantation.MethodsIn total, 252 patients who underwent kidney transplantation were enrolled in this study. Antibodies for human leukocyte antigens (HLAs) and non-HLAs were analyzed immediately before transplantation. Patients were categorized based on the occurrence of antibody-mediated rejection (AMR) or T-cell-mediated rejection (TCMR) by 2017 Banff classification. All p-values were two-tailed, and statistical significance was set at p < 0.05.ResultsPatients with anti-AT1R antibodies had a 3.49-fold higher risk of TCMR than those without anti-AT1R antibodies. Patients with anti-ETAR antibodies had a 5.84-fold higher risk of AMR than those without anti-ETAR antibodies. The hazard ratio of AMR in patients with both HLA DSAs and anti-ETAR antibodies, relative to patients without anti-ETAR antibodies and HLA DSAs, was 32.85 (95% CI = 1.82-592.91).ConclusionOur findings indicated that anti-ETAR antibodies are associated with AMR, and patients with both anti-ETAR antibodies and de novo HLA DSAs were at a high risk of AMR.

| S-EPMC10561590 | biostudies-literature

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