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Updated: Jul 10, 2026

Mouse Kidney Transplantation: Models of Allograft Rejection

Mouse Kidney Transplantation: Models of Allograft Rejection

Published on: October 11, 2014

Microarray analysis of rejection in human kidney transplants using pathogenesis-based transcript sets.

T F Mueller¹, G Einecke, J Reeve

¹Department of Medicine, Division of Nephrology and Immunology, University of Alberta, Edmonton, AB, Canada.

American Journal of Transplantation : Official Journal of the American Society of Transplantation and the American Society of Transplant Surgeons

|October 19, 2007

Summary

This summary is machine-generated.

Pathogenesis-based transcript sets (PBTs) reveal a continuous spectrum of inflammatory disturbances in organ transplants, aiding objective diagnosis of allograft rejection. These molecular signatures correlate with histopathology and clinical outcomes, offering new insights into rejection mechanisms.

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Measurement of T Cell Alloreactivity Using Imaging Flow Cytometry

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Last Updated: Jul 10, 2026

Mouse Kidney Transplantation: Models of Allograft Rejection

Mouse Kidney Transplantation: Models of Allograft Rejection

Published on: October 11, 2014

Measurement of T Cell Alloreactivity Using Imaging Flow Cytometry

Measurement of T Cell Alloreactivity Using Imaging Flow Cytometry

Published on: April 19, 2017

Area of Science:

Transplant immunology
Molecular diagnostics
Genomics

Background:

Microarrays can objectively diagnose allograft rejection and elucidate pathogenesis.
Pathogenesis-based transcript sets (PBTs) capture key rejection events: T-cell infiltration, interferon-gamma effects, and parenchymal damage.

Purpose of the Study:

To correlate PBT expression with histopathology and clinical diagnoses in human kidney transplant biopsies.
To investigate the internal structure and continuity of transcriptome disturbances in allograft rejection.

Main Methods:

Analysis of 143 human kidney transplant biopsies using microarrays to define PBTs.
Correlation of PBT expression with histopathologic findings and clinical rejection status.
Validation of findings in an additional 51 biopsies.

Main Results:

PBTs showed strong inter-correlation, indicating a structured transcriptome disturbance in rejection.
Transcriptome disturbance was continuous across rejection and non-rejection states.
PBTs correlated with histopathology and were highest during clinical rejection episodes; antibody-mediated rejection showed similar patterns to T-cell mediated rejection.
Absence of PBT disturbance indicated no rejection, and PBTs questioned the reliability of some Banff criteria.

Conclusions:

PBTs provide a quantitative measure of inflammatory disturbances in organ transplants.
Transcriptome changes reflect a large-scale disturbance characteristic of rejection, present at varying levels in different injury types.
PBTs offer a novel perspective on transplant rejection mechanisms and diagnostics.