Abstract
The protective immune response against liver stages of the malaria parasite critically requires CD8(+) T cells. Although the nature of the effector mechanism utilized by these cells to repress parasite development remains unclear, a critical role for gamma interferon (IFN-gamma) has been widely assumed based on circumstantial evidence. However, the requirement for CD8(+) T-cell-mediated IFN-gamma production in protective immunity to this pathogen has not been directly tested. In this report, we use an adoptive transfer strategy with circumsporozoite (CS) protein-specific transgenic T cells to examine the role of CD8(+) T-cell-derived IFN-gamma production in Plasmodium yoelii-infected mice. We show that despite a marginal reduction in the expansion of naive IFN-gamma-deficient CS-specific transgenic T cells, their antiparasite activity remains intact. Further, adoptively transferred IFN-gamma-deficient CD8(+) T cells were as efficient as their wild-type counterparts in limiting parasite growth in naive mice. Taken together, these studies demonstrate that IFN-gamma secretion by CS-specific CD8(+) T cells is not essential to protect mice against live sporozoite challenge.