T-cell alloimmunity and chronic allograft dysfunction

    Research output: Contribution to journalLiterature reviewpeer-review

    50 Citations (Scopus)


    Solid organ transplantation is the standard treatment to improve both the quality of life and survival in patients with various end-stage organ diseases. The primary barrier against successful transplantation is recipient alloimmunity and the need to be maintained on immunosuppressive therapies with associated side effects. Despite such treatments in renal transplantation, after death with a functioning graft, chronic allograft dysfunction (CAD) is the most common cause of late allograft loss. Recipient recognition of donor histocompatibility antigens, via direct, indirect, and semidirect pathways, is critically dependent on the antigen-presenting cell (APC) and elicits effector responses dominated by recipient T cells. In allograft rejection, the engagement of recipient and donor cells results in recruitment of T-helper (Th) cells of the Th1 and Th17 lineage to the graft. In cases in which the alloresponse is dominated by regulatory T cells (Tregs), rejection can be prevented and the allograft tolerated with minimum or no immunosuppression. Here, we review the pathways of allorecognition that underlie CAD and the T-cell effector phenotypes elicited as part of the alloresponse. Future therapies including depletion of donor-reactive lymphocytes, costimulation blockade, negative vaccination using dendritic cell subtypes, and Treg therapy are inferred from an understanding of these mechanisms of allograft rejection.
    Original languageEnglish
    Article numberN/A
    Pages (from-to)S2 - S12
    Number of pages11
    JournalKidney International
    Issue numberSUPPL. 119
    Publication statusPublished - Dec 2010


    • Animals
    • Chronic Disease
    • Graft Rejection
    • Histocompatibility
    • Humans
    • Immunosuppression
    • Isoantigens
    • Kidney
    • Kidney Diseases
    • Kidney Transplantation
    • T-Lymphocytes
    • Transplantation, Homologous
    • Treatment Outcome


    Dive into the research topics of 'T-cell alloimmunity and chronic allograft dysfunction'. Together they form a unique fingerprint.

    Cite this