Summary. Given the known role of the fas cytolytic pathway in B-cell regulation, we evaluated whether fas±fasL interactions might induce chronic lymphocytic leukaemia (CLL) cell death. De novo CLL cells expressed a low level of surface fas, and were not lysed by fasL-bearing cells. CLL cells cultured in media containing the type I cytokines interleukin (IL)-12 or interferon (IFN)-a had increased fas expression, and were readily lysed by fasL-bearing cells. In contrast, the type II cytokine IL-4 did not increase CLL cell fas, and abrogated type I cytokine-induced fas up-regulation. With prolonged culture, IL-4 exposed CLL cells expressed an intermediate level of fas; however, such CLL cells were resistant to fas-mediated lysis. These results indicate that IL-4 inhibits fas-mediated killing of CLL cells at the level of both fas receptor expression and post-receptor events. Additionally, we have de®ned in vitro culture conditions which generate fasL-bearing T cells from CLL patients; such T cells ef®ciently mediated fas-based lysis of autologous fas-positive CLL cells. We therefore conclude that type I and type II cytokines differentially regulate the fas pathway in CLL cells, and that a combination of type I cytokines and fasL-expressing T cells may represent a new approach to the immunotherapy of CLL.

TRE was not as severely impaired as anticipated and was variable based on plane of measure. Time in a rehabilitation setting produced significant improvements in functional outcomes but TRE improvements were not as robust. These results indicate a need for further investigation of the strength of the interrelationship between TRE and function.

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