PD-1 blockade promotes immune memory following Plasmodium berghei ANKA reinfection

The establishment of malaria immune memory is slow, incomplete, and short-lived. The mechanisms underpinning the generation and maintenance of anti-malarial immune memory remain unclear. This study evaluated the possible role of programmed cell death-1 (PD-1) in the establishment of malaria immune memory. Following infection by Plasmodium berghei ANKA (Pb ANKA) we compared natural immunity, acquired immunity, and immune memory between WT and mice lacking PD-1 via monoclonal antibody treatment. We found that parasitemia levels were significantly lower in the PD-1 knockdown group. After PD-1 elimination, dendritic cells, Th1, and T-follicular helper cells increased significantly. In addition, memory T, long-lived plasma cells, and serum antibody production also increased significantly. Therefore, PD-1 elimination induced stronger natural and acquired immune responses and enhanced immune memory against the parasite.