Pathogenesis of chronic allograft rejection

Chronic allograft nephropathy (CAN) is, besides death of the recipient with graft function, the most common cause of renal transplant loss. It is characterized by loss of function and replacement of tissue by fibrotic material. The pathogenesis is not clear, but seems to be multifactorial and involv...

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Bibliographic Details
Published in:Transplant international 2003-03, Vol.16 (3), p.137-145
Main Authors: Joosten, Simone A., Kooten, Cees, Paul, Leendert C.
Format: Article
Language:English
Subjects:
Acute Disease
Antibodies
Biological and medical sciences
Chronic Disease
Chronic rejection
Combined surgery. Multiple transplantations
Graft Rejection - immunology
Graft Rejection - physiopathology
Graft Rejection - prevention & control
Humans
Immunosuppressive Agents - therapeutic use
Indirect presentation
Kidney Transplantation - adverse effects
Kidney Transplantation - immunology
Medical sciences
Models, Immunological
Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases
Tissue‐specific
Transplantation
Transplantation, Homologous - immunology
Transplantation, Homologous - physiology
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Summary:Chronic allograft nephropathy (CAN) is, besides death of the recipient with graft function, the most common cause of renal transplant loss. It is characterized by loss of function and replacement of tissue by fibrotic material. The pathogenesis is not clear, but seems to be multifactorial and involves events both early and late after transplantation. Alloantigen‐dependent mechanisms seem to be crucial for the deveopment of chronic rejection (CR). Although modern immunosuppressive drugs have reduced the number and severity of acute rejection episodes, their effects on CR are less obvious. In this review we discuss the role of direct and indirect antigen presentation in the development of CR, and we will focus on the production of antibodies directed against HLA and non‐HLA antigens on the graft and their influence on CR.
ISSN:0934-0874
1432-2277
DOI:10.1111/j.1432-2277.2003.tb00277.x