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  ).