Autologous lymphokine-activated killer cell therapy of lymphoproliferative disorders arising in organ transplant recipients.

B CELL lymphomas which often contain the EpsteinBarr virus (EBY) make up the preponderance of tumors that collectively have been tcrmed posttransplant Iymphoproliferative disordcrs (PTLD). The unusual susceptibility of PTLD to immune surveillance was first demonstrated in organ allograft recipients following reduction (or discontinuance) of immunosuppression I with its attendant risk of precipitating allograft rejection. Restoration of tumor surveillance has rccently been accomplished in bone marrow transplant recipients with PTLD by infusing naive cytotoxic T lymphocytes (CfL) obtained from the original donors into the tumor-bearing recipients. In these cases the tumors are invariably of donor origin, and HLA-restricted effector cells directed against viral targets are thought to be the main mediators of tumor regression.~·:1 The unavailability of naive pretransplant recipient leukocytes has precluded direct application of this technology to the PTLDs which develop after organ transplantation and which are almost always of recipient origin.4 However, we report herein an approach whereby the antiPTLD activity of the recipient's own cells can be intensified in vitro. Reinfusion of these cells has been associated with clinical tumor regression in several cases.