Expression data from malaria-specific mouse CD4 T cell (PbT-II) subset after Plasmodium berghei ANKA infection

The multiple species of Plasmodium that infect humans are highly polymorphic and induce various infections ranging from asymptomatic state to severe life-threatening diseases such as cerebral malaria. However, how the differences between the parasites affect host immune responses during blood-stage infection remains largely unknown. In this study, we investigated the CD4+ T-cell immune responses in T-cell receptor-transgenic mice infected simultaneously with P. berghei ANKA (PbA) and P. chabaudi chabaudi AS (Pcc) using PbT-II cells, which recognize a common epitope of these parasites. In the acute phase of infection, CD4+ T-cell responses in PbA-infected mice showed a higher involvement of Th1 cells and a lower proportion of Ly6Clo effector CD4+ T cells than those in Pcc-infected mice. Transcriptome analysis of PbT-II cells indicated that type I interferon (IFN)-regulated genes were expressed at higher levels in both Th1- and Tfh-type PbT-II cells from PbA-infected mice than those from Pcc-infected mice. Moreover, IFN-α levels were considerably higher in PbA-infected mice than in Pcc-infected mice. Inhibition of type I IFN signaling increased PbT-II and Ly6Clo cell numbers and partially reversed the Th1 over Tfh bias of the PbT-II cells in both PbA- and Pcc-infected mice. However, in the memory phase, we did not find a significant difference in the phenotype of PbT-II cells between PbA- and Pcc-primed mice. These observations suggested that the differences in Plasmodium-specific CD4+ T-cell responses between PbA- and Pcc-infected mice were at least partially associated with the difference in type I cytokine production during the early phase of the infection. PbT-II cells underwent adoptive transfer into B6 mice and infected with Plasmodium berghei ANKA. Seven days after infection, we sorted subsets of PbT-II cells based on their expression of CD11a and CD49d expression.