Mechanisms of allograft rejection
Direct, indirect and semi-direct allorecognition, the three-signal model of T-cell activation and where each immunosuppressant acts, and the timing, mechanism and Banff biopsy features of hyperacute, T-cell-mediated, antibody-mediated and chronic rejection.
Tier 2Medical sciences concept
Written with AI assistance and fact-checked against the sources below. For exam study, not clinical decisions. How notes are made
At a glance
- Rejection is driven by HLA disparity and the very high frequency of T cells that recognise foreign HLA (up to 10% of the repertoire).
- Two arms: T-cell-mediated rejection (TCMR) and antibody-mediated rejection (ABMR). ABMR is now the main cause of late kidney graft loss.
- Immunosuppressants map onto the three-signal model of T-cell activation. Paper 1 asks which drug blocks which step.
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Sources
- KDIGO clinical practice guideline for the care of kidney transplant recipientsKidney Disease Improving Global Outcomes (American Journal of Transplantation 2009;9 Suppl 3), 2009 (predates current Banff ABMR criteria)
- Recommended treatment for antibody-mediated rejection after kidney transplantation: the 2019 expert consensus from the Transplantation Society Working GroupTransplantation (Schinstock et al.) 2020;104:911-22, 2020
- The Banff 2022 Kidney Meeting Report: reappraisal of microvascular inflammation and the role of biopsy-based transcript diagnosticsAmerican Journal of Transplantation (Naesens et al.), 2024
- Clinical guidelines for organ transplantation from deceased donorsAU/NZTransplantation Society of Australia and New Zealand (TSANZ)
- ANZDATA Registry annual report: kidney transplantationAU/NZAustralia and New Zealand Dialysis and Transplant Registry
- Janeway's Immunobiology (10th ed.)W. W. Norton (Murphy and Weaver), 2022
- Last updated
- 14 November 2026
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