γδ T-cell function in pathogenesis of cerebral malaria in mice infected with Plasmodium berghei ANKA

Abstract

Mice depleted of γδ T cells by monoclonal antibody treatment and infected with Plasmodium berghei ANKA did not develop cerebral malaria (CM). In striking contrast, δ(0/0) mice infected with P. berghei developed CM despite their γδ T-cell deficiency. γδ T cells appear to be essential for the pathogenesis of CM in mice having experienced normal ontogeny but not in mice genetically deprived of γδ T cells from the beginning of life.