This discussion has sought to identify the known alterations in immune cell function associated with B-CLL. The elucidation of the underlying mechanisms for the abnormal cell immune func tioning in B-CLL has provided further targets for therapeutic intervention. For example, the identification of the defective CD40/CD154 interaction leading to poor APC ability has resulted in the design and introduction of gene therapy intended to make the leukemic cells "visible" to the innate immune system. Other opportunities include the judicious exploration and testing of cytokines such as IL-2 to improve NK function or interruption of cytokine pathways like IL-4 that impact on CLL B-cell apoptosis. Newer technologies, including gene array profiling, may lgive us insight into the nature of the complex interplay between cells in the immune system. Innovative strategies designed to treat B-CLL appearing on the near horizon include peptide and cellular vaccines and the use of cytokines or donor lymphocyte infusions. Given that these vaccines require a competent immune system to yield optimum clinical results, we need to develop strategies specifically designed to activate, enhance, and replete the host immune system. This latter activity probably represents the most significant challenge in our long-term management and care of B-CLL patients.
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