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Significance Cerebral malaria (CM) is a potentially fatal neurological complication caused byPlasmodium falciparum affecting mainly young children. In endemic areas, severe complications become less frequent as γδ-T cell responses decline. However, the role of γδ-T cells in CM pathogenesis remains unclear. Here, we show that mice deficient in γδ-T cells are resistant to experimental CM development when infected withPlasmodium berghei ANKA sporozoites. Importantly, we demonstrate that the presence of γδ-T cells enhanced the expression ofPlasmodium immunogenic factors upon liver-stage infection and promoted subsequent blood-stage inflammatory responses. This study characterizes a critical pathogenic role of γδ-T cells in experimental CM that provides a strong rationale for their modulation toward achieving “clinical immunity” to malaria.

γδ-T cells promote IFN-γ–dependentPlasmodiumpathogenesis upon liver-stage infection