CD4+ T cells play an important role in immunity to blood-stage malaria parasites and in disease pathogenesis. The role of CD4+T cells has been demonstrated by selective depletion in vitro (1 -3 ), by adoptive transfer of T cells to immunodeficient mice (1 ,4 -7 ), and by the ability of human T cells to inhibit parasite growth in vitro (8 ). Both types of CD4+ T cells (Th1 and Th2) have been shown to be effective in malaria infection (6 ). Factors that affect cell activation, function, and life-span of parasite-specific T cells would be expected to have a significant impact on parasite survival, including the poor immunogenicity of parasite antigens (9 ), antigenic polymorphism (10 -12 ), immunosuppression as a result of malaria infection (13 ), and the need for continuous malaria exposure to maintain immunological memory (14 ). Antigen-driven deletion or anergy of immunological responses is a major regulatory strategy to control potentially harmful responses (15 ) and may be used by infectious organisms to their advantage, as shown by the exhaustive deletion of lymphocytic choriomeningitis virus-specific CD8+ T cells (16 ), and the deletion of Plasmodium berghei-specific T cells after adoptive transfer into immunodeficient mice (17 ).