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17 - Immunological mechanisms of graft injury
- Edited by Nicholas R. Banner, Julia M. Polak, Imperial College of Science, Technology and Medicine, London, Magdi H. Yacoub, University of London
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- Book:
- Lung Transplantation
- Published online:
- 06 January 2010
- Print publication:
- 15 May 2003, pp 185-204
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Summary
Overview
In the clinical situation the vast majority of transplants are allografts, organs transplanted between genetically different individuals of the same species. These will be the focus of this chapter. However, the future may hold the option of xenografting where organs are transplanted from one species to another. Commercial and other considerations have dictated the choice of the pig as a potential donor for humans. Where appropriate, mention will be made of xenotransplantation.
Graft rejection is often categorized according to the tempo at which it happens. The terms hyperacute, acute and chronic rejection are used to describe graft damage that occurs in minutes to hours, days to weeks, or months to years after transplantation, respectively [1]. However, the mechanisms responsible for acute rejection may be activated late after transplantation, while the changes characteristic of chronic rejection may be seen very early after transplantation in some recipients. Hence it is generally better to think in terms of the underlying mechanisms and accept that the immune system will do its utmost, using almost every specific and nonspecific mechanism it can muster, to destroy the transplanted tissue. In general, if steps were not taken to overcome the mechanisms of rejection then the majority of grafts would be lost very quickly.
To complicate matters, the graft itself responds to the transplantation procedure and to its new and often hostile environment. The period of cold ischaemia during the transplantation procedure elicits the expression of a range of new molecules, including adhesion molecules, proinflammatory cytokines and chemokines. These serve to promote the infiltration of the graft by recipient leukocytes, first by neutrophils, followed by monocytes and macrophages then ultimately by lymphocytes.
18 - Role of endothelial cells in transplant rejection
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- By Marlene L. Rose, Division of Cardiothoracic Surgery, Imperial College School of Medicine, Harefield, Middlesex
- Edited by Beverley J. Hunt, University of London, Lucilla Poston, University of London, Michael Schachter, Imperial College of Science, Technology and Medicine, London, Alison W. Halliday, St George's Hospital, London
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- Book:
- An Introduction to Vascular Biology
- Published online:
- 07 September 2009
- Print publication:
- 25 July 2002, pp 381-397
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Summary
Introduction
Approximately 36 000 transplants are performed throughout the world each year, of which the majority are kidney transplants. About 5000 hearts, 6500 livers and 1200 lung transplants are performed. Rejection remains the most common complication following transplantation and is the major cause of morbidity and mortality. Endothelial cells form the interface between donor tissue and recipient blood and so are the first donor cells to be recognized by the host's immune system. This fact, and the observation that they express numerous molecules able to stimulate lymphocytes, has led to much research into their precise role in transplant rejection. It is our view that endothelial cells are pivotal both in controlling the egress of inflammatory cells into the allografted organ and also as specific antigen-presenting cells (APCs), by presenting foreign molecules to the immune system (Figure 18.1).
Rejection is mediated by both cell-mediated and humoral mechanisms but the relative importance of these pathways differs in acute and chronic rejection. This chapter briefly describes the features of acute and chronic rejection and then outlines the role of endothelial cells in this process.
Basic mechanism of rejection
The major stimulus for rejection of allografted organs is recognition that the donor cells are foreign, by recognition of antigens that are coded by the major histocompatibility complex (MHC). There are two classes of MHC: class I (human leukocyte antigen, HLA) ABC) and class II (HLA-DR, DP, DQ).
41 - Monitoring heart and lung transplant patients
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- By Marlene L. Rose, Harefield Hospital, Harefield, UK
- Edited by Andrew K. Trull, Lawrence M. Demers, David W. Holt, Atholl Johnston, J. Michael Tredger, Christopher P. Price
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- Book:
- Biomarkers of Disease
- Published online:
- 20 August 2009
- Print publication:
- 06 June 2002, pp 415-422
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Summary
Introduction
Approximately 10 000 hearts and 2000 lungs are transplanted every year. Rejection remains the most common complication following transplantation and is the major source of morbidity and mortality. Constant vigilance is required to monitor the immune response to the grafted organ in the first 3 months, when acute rejection is most likely to occur. In contrast to the management of kidney transplant recipients, in whom raised levels of serum creatinine and urea can be used to monitor graft function, monitoring the function of transplanted hearts and lungs relies entirely on histological or clinical parameters.
Thus, for patients who have undergone cardiac transplantation, surveillance endomyocardial biopsies are taken at weekly intervals for the first 6 weeks and then at 2-weekly intervals until the end of the third postoperative month. In addition, any positive biopsy is followed up by a repeat biopsy 1 week later to ensure that antirejection therapy has been successful. Patients also undergo further biopsies when clinically indicated. Thus, every heart transplant patient has a minimum of nine biopsy procedures within the first postoperative year. Lung allograft function is monitored daily by the patients themselves by means of a spirometer. Any unexplained persistent fall in the forced expiratory volume will be followed up by transbronchial biopsy to confirm the diagnosis histologically. It is especially important to obtain a differential diagnosis between rejection and infection after lung transplantation. For this reason, the transbronchial biopsy procedure is usually accompanied by bronchoalveolar lavage, which is sent for culture and microbiological analysis.
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