Abstract
Post-transplantation lymphoproliferative disorder (PTLD) is a frequently fatal complication of immunosuppression [1]. The term describes Epstein–Barr virus associated B-lymphoproliferations occurring after organ transplantation. The disease has assumed increasing clinical importance in view of the constantly rising number of organ transplant recipients and the development of highly potent and specific immunosuppressive drugs. Continued, uncontrolled EBV-driven proliferation of B-cells in the absence of adequate T-cell control has been proposed as a mechanism for the development of PTLD by Klein and others [2, 3]. As proliferation continues, clones with a growth advantage emerge, and a monoclonal population eventually predominates. This model is capable of at least partially explaining many of the otherwise puzzling clinical and pathologic features of this disease.
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© 1996 Kluwer Academic Publishers
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Swinnen, L.J. (1996). Increased risk of lymphoproliferative disorders following the use of OKT3: Association with cumulative dose. In: Touraine, J.L., Traeger, J., Bétuel, H., Dubernard, J.M., Revillard, J.P., Dupuy, C. (eds) Cancer in Transplantation: Prevention and Treatment. Transplantation and Clinical Immunology, vol 27. Springer, Dordrecht. https://doi.org/10.1007/978-94-009-0175-9_28
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DOI: https://doi.org/10.1007/978-94-009-0175-9_28
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